mers-structure.bib

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@misc{mers-structure,
	Author = {Dudas, Gytis},
	Copyright = {CC-BY-SA-4.0},
	Date-Added = {2017-12-12 23:29:20 +0000},
	Date-Modified = {2017-12-12 23:37:19 +0000},
	File = {Snapshot:/Users/evogytis/Zotero/storage/H7FY5DXN/mers-structure.html:text/html},
	Howpublished = {b1fe9abbd633222342f7850ec01a494812e2ca9b},
	Month = aug,
	Publisher = {Bedford Lab},
	Shorttitle = {mers-structure},
	Title = {mers-structure: {Looking} into {MERS}-{CoV} dynamics through the structured coalescent lens},
	Url = {https://github.com/blab/mers-structure},
	Urldate = {2017-12-12},
	Year = {2017},
	Bdsk-Url-1 = {https://github.com/blab/mers-structure}}

@article{rasmussen_phylodynamic_2014,
	Abstract = {Author Summary Mathematical models play an important role in our understanding of what processes drive the complex population dynamics of infectious pathogens. Yet developing statistical methods for fitting models to epidemiological data is difficult. Epidemiological data is often noisy, incomplete, aggregated across different scales and generally provides only a partial picture of the underlying disease dynamics. Using nontraditional sources of data, like molecular sequences of pathogens, can provide additional information about epidemiological dynamics. But current ``phylodynamic'' inference methods for fitting models to genealogies reconstructed from sequence data have a number of major limitations. We present a statistical framework that builds upon earlier work to address two of these limitations: population structure and stochasticity. By incorporating population structure, our framework can be applied in cases where the host population is divided into different subpopulations, such as by spatial isolation. Our framework also takes into consideration stochastic noise and can therefore capture the inherent variability of epidemiological dynamics. These advances allow for a much wider class of epidemiological models to be fit to genealogies in order to estimate key epidemiological parameters and to reconstruct past disease dynamics.},
	Author = {Rasmussen, David A. and Volz, Erik M. and Koelle, Katia},
	Date-Added = {2017-11-22 21:43:21 +0000},
	Date-Modified = {2017-11-22 21:43:21 +0000},
	Doi = {10.1371/journal.pcbi.1003570},
	File = {Full Text PDF:/Users/evogytis/Zotero/storage/2RVD7HVU/Rasmussen et al. - 2014 - Phylodynamic Inference for Structured Epidemiologi.pdf:application/pdf;Snapshot:/Users/evogytis/Zotero/storage/B7LBIVJT/article.html:text/html},
	Issn = {1553-7358},
	Journal = {PLOS Computational Biology},
	Keywords = {Epidemiology, Algorithms, HIV, HIV epidemiology, Infectious disease epidemiology, Pathogens, Population density, Population dynamics},
	Month = apr,
	Number = {4},
	Pages = {e1003570},
	Title = {Phylodynamic {Inference} for {Structured} {Epidemiological} {Models}},
	Url = {http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003570},
	Urldate = {2017-11-22},
	Volume = {10},
	Year = {2014},
	Bdsk-Url-1 = {http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003570},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pcbi.1003570}}

@article{frost_viral_2010,
	Author = {Frost, Simon DW and Volz, Erik M},
	Date-Added = {2017-11-22 01:07:16 +0000},
	Date-Modified = {2017-11-22 01:08:04 +0000},
	Journal = {Philos Trans Royal Soc B Trans R Soc B},
	Number = {1548},
	Pages = {1879--1890},
	Title = {Viral phylodynamics and the search for an `effective number of infections'},
	Volume = {365},
	Year = {2010}}

@article{lipsitch_viral_2016,
	Author = {Lipsitch, Marc and Barclay, Wendy and Raman, Rahul and Russell, Charles J and Belser, Jessica A and Cobey, Sarah and Kasson, Peter M and Lloyd-Smith, James O and Maurer-Stroh, Sebastian and Riley, Steven and others},
	Date-Added = {2017-11-21 23:06:10 +0000},
	Date-Modified = {2017-11-21 23:06:27 +0000},
	Journal = {eLife},
	Pages = {e18491},
	Title = {Viral factors in influenza pandemic risk assessment},
	Volume = {5},
	Year = {2016}}

@article{park_multiple_2013,
	Author = {Park, Miran and Loverdo, Claude and Schreiber, Sebastian J and Lloyd-Smith, James O},
	Date-Added = {2017-11-21 22:53:51 +0000},
	Date-Modified = {2017-11-21 22:54:53 +0000},
	Journal = {Philos Trans Royal Soc B},
	Number = {1614},
	Pages = {20120333},
	Title = {Multiple scales of selection influence the evolutionary emergence of novel pathogens},
	Volume = {368},
	Year = {2013}}

@article{kuhnert_phylodynamics_2016,
	Abstract = {When viruses spread, outbreaks can be spawned in previously unaffected regions. Depending on the time and mode of introduction, each regional outbreak can have its own epidemic dynamics. The migration and phylodynamic processes are often intertwined and need to be taken into account when analyzing temporally and spatially structured virus data. In this article, we present a fully probabilistic approach for the joint reconstruction of phylodynamic history in structured populations (such as geographic structure) based on a multitype birth--death process. This approach can be used to quantify the spread of a pathogen in a structured population. Changes in epidemic dynamics through time within subpopulations are incorporated through piecewise constant changes in transmission parameters.We analyze a global human influenza H3N2 virus data set from a geographically structured host population to demonstrate how seasonal dynamics can be inferred simultaneously with the phylogeny and migration process. Our results suggest that the main migration path among the northern, tropical, and southern region represented in the sample analyzed here is the one leading from the tropics to the northern region. Furthermore, the time-dependent transmission dynamics between and within two HIV risk groups, heterosexuals and injecting drug users, in the Latvian HIV epidemic are investigated. Our analyses confirm that the Latvian HIV epidemic peaking around 2001 was mainly driven by the injecting drug user risk group.},
	Author = {K{\"u}hnert, Denise and Stadler, Tanja and Vaughan, Timothy G. and Drummond, Alexei J.},
	Date-Added = {2017-11-09 20:11:12 +0000},
	Date-Modified = {2017-11-09 20:11:12 +0000},
	Doi = {10.1093/molbev/msw064},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/3VVUNG63/K{\"u}hnert et al. - 2016 - Phylodynamics with Migration A Computational Fram.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/HNRP2ZWM/2578541.html:text/html},
	Issn = {0737-4038},
	Journal = {Molecular Biology and Evolution},
	Month = aug,
	Number = {8},
	Pages = {2102--2116},
	Shorttitle = {Phylodynamics with {Migration}},
	Title = {Phylodynamics with {Migration}: {A} {Computational} {Framework} to {Quantify} {Population} {Structure} from {Genomic} {Data}},
	Url = {https://academic.oup.com/mbe/article/33/8/2102/2578541},
	Urldate = {2017-11-09},
	Volume = {33},
	Year = {2016},
	Bdsk-Url-1 = {https://academic.oup.com/mbe/article/33/8/2102/2578541},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msw064}}

@article{guindon_simple_2003,
	Abstract = {The increase in the number of large data sets and the complexity of current probabilistic sequence evolution models necessitates fast and reliable phylogeny reconstruction methods. We describe a new approach, based on the maximum-likelihood principle, which clearly satisfies these requirements. The core of this method is a simple hill-climbing algorithm that adjusts tree topology and branch lengths simultaneously. This algorithm starts from an initial tree built by a fast distance-based method and modifies this tree to improve its likelihood at each iteration. Due to this simultaneous adjustment of the topology and branch lengths, only a few iterations are sufficient to reach an optimum. We used extensive and realistic computer simulations to show that the topological accuracy of this new method is at least as high as that of the existing maximum-likelihood programs and much higher than the performance of distance-based and parsimony approaches. The reduction of computing time is dramatic in comparison with other maximum-likelihood packages, while the likelihood maximization ability tends to be higher. For example, only 12 min were required on a standard personal computer to analyze a data set consisting of 500 rbc L sequences with 1,428 base pairs from plant plastids, thus reaching a speed of the same order as some popular distance-based and parsimony algorithms. This new method is implemented in the PHYML program, which is freely available on our web page: http://www.lirmm.fr/w3ifa/MAAS/.},
	Author = {Guindon, St{\'e}phane and Gascuel, Olivier and Rannala, Bruce},
	Date-Added = {2017-11-07 19:35:47 +0000},
	Date-Modified = {2017-11-07 19:35:47 +0000},
	Doi = {10.1080/10635150390235520},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/NH3WGPPR/Guindon et al. - 2003 - A Simple, Fast, and Accurate Algorithm to Estimate.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/WICB2ERW/1681984.html:text/html},
	Issn = {1063-5157},
	Journal = {Systematic Biology},
	Month = oct,
	Number = {5},
	Pages = {696--704},
	Title = {A {Simple}, {Fast}, and {Accurate} {Algorithm} to {Estimate} {Large} {Phylogenies} by {Maximum} {Likelihood}},
	Url = {https://academic.oup.com/sysbio/article/52/5/696/1681984},
	Urldate = {2017-11-07},
	Volume = {52},
	Year = {2003},
	Bdsk-Url-1 = {https://academic.oup.com/sysbio/article/52/5/696/1681984},
	Bdsk-Url-2 = {http://dx.doi.org/10.1080/10635150390235520}}

@article{heled_looking_2013,
	Abstract = {Bayesian phylogenetic analysis generates a set of trees which are often condensed into a single tree representing the whole set. Many methods exist for selecting a representative topology for a set of unrooted trees, few exist for assigning branch lengths to a fixed topology, and even fewer for simultaneously setting the topology and branch lengths. However, there is very little research into locating a good representative for a set of rooted time trees like the ones obtained from a BEAST analysis.},
	Annote = {Pages 221 in PDF},
	Author = {Heled, Joseph and Bouckaert, Remco R.},
	Date-Added = {2017-10-30 22:37:04 +0000},
	Date-Modified = {2017-10-30 22:37:04 +0000},
	Doi = {10.1186/1471-2148-13-221},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/M5SNZ7J5/Heled and Bouckaert - 2013 - Looking for trees in the forest summary tree from.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/GU4K4ACE/1471-2148-13-221.html:text/html},
	Issn = {1471-2148},
	Journal = {BMC Evolutionary Biology},
	Month = oct,
	Pages = {221},
	Shorttitle = {Looking for trees in the forest},
	Title = {Looking for trees in the forest: summary tree from posterior samples},
	Url = {https://doi.org/10.1186/1471-2148-13-221},
	Volume = {13},
	Year = {2013},
	Bdsk-Url-1 = {https://doi.org/10.1186/1471-2148-13-221},
	Bdsk-Url-2 = {http://dx.doi.org/10.1186/1471-2148-13-221}}

@article{lemey_bayesian_2009,
	Abstract = {Author Summary Spreading in time and space, rapidly evolving viruses can accumulate a considerable amount of genetic variation. As a consequence, viral genomes become valuable resources to reconstruct the spatial and temporal processes that are shaping epidemic or endemic dynamics. In molecular epidemiology, spatial inference is often limited to the interpretation of evolutionary histories with respect to the sampling locations of the pathogens. To test hypotheses about the spatial diffusion patterns of viruses, analytical techniques are required that enable us to reconstruct how viruses migrated in the past. Here, we develop a model to infer diffusion processes among discrete locations in timed evolutionary histories in a statistically efficient fashion. Applications to Avian Influenza A H5N1 and Rabies virus in Central and West African dogs demonstrate several advantages of simultaneously inferring spatial and temporal processes from gene sequences.},
	Author = {Lemey, Philippe and Rambaut, Andrew and Drummond, Alexei J. and Suchard, Marc A.},
	Date-Added = {2017-10-30 21:13:47 +0000},
	Date-Modified = {2017-10-30 21:13:47 +0000},
	Doi = {10.1371/journal.pcbi.1000520},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/KEHDTXRA/Lemey et al. - 2009 - Bayesian Phylogeography Finds Its Roots.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/VJ7TECF7/article.html:text/html},
	Issn = {1553-7358},
	Journal = {PLOS Computational Biology},
	Keywords = {Animal phylogenetics, Avian influenza, Evolutionary genetics, Phylogenetic analysis, Phylogenetics, Phylogeography, Rabies virus, Viral evolution},
	Month = sep,
	Number = {9},
	Pages = {e1000520},
	Title = {Bayesian {Phylogeography} {Finds} {Its} {Roots}},
	Url = {http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1000520},
	Urldate = {2017-10-30},
	Volume = {5},
	Year = {2009},
	Bdsk-Url-1 = {http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1000520},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pcbi.1000520}}

@article{antia_role_2003,
	Abstract = {It is unclear when, where and how novel pathogens such as human immunodeficiency virus (HIV), monkeypox and severe acute respiratory syndrome (SARS) will cross the barriers that separate their natural reservoirs from human populations and ignite the epidemic spread of novel infectious diseases. New pathogens are believed to emerge from animal reservoirs when ecological changes increase the pathogen's opportunities to enter the human population and to generate subsequent human-to-human transmission. Effective human-to-human transmission requires that the pathogen's basic reproductive number, R0, should exceed one, where R0 is the average number of secondary infections arising from one infected individual in a completely susceptible population. However, an increase in R0, even when insufficient to generate an epidemic, nonetheless increases the number of subsequently infected individuals. Here we show that, as a consequence of this, the probability of pathogen evolution to R0 {\textgreater} 1 and subsequent disease emergence can increase markedly.},
	Author = {Antia, Rustom and Regoes, Roland R. and Koella, Jacob C. and Bergstrom, Carl T.},
	Copyright = {{\copyright} 2003 Nature Publishing Group},
	Date-Added = {2017-10-23 21:25:34 +0000},
	Date-Modified = {2017-10-23 21:25:34 +0000},
	Doi = {10.1038/nature02104},
	File = {Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/DZHFHF73/nature02104.html:text/html},
	Issn = {0028-0836},
	Journal = {Nature},
	Language = {en},
	Month = dec,
	Number = {6967},
	Pages = {658--661},
	Title = {The role of evolution in the emergence of infectious diseases},
	Url = {https://www.nature.com/nature/journal/v426/n6967/full/nature02104.html},
	Urldate = {2017-10-23},
	Volume = {426},
	Year = {2003},
	Bdsk-Url-1 = {https://www.nature.com/nature/journal/v426/n6967/full/nature02104.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature02104}}

@article{volz_complex_2011,
	Abstract = {Estimates of the coalescent effective population size Ne can be poorly correlated with the true population size. The relationship between Ne and the population size is sensitive to the way in which birth and death rates vary over time. The problem of inference is exacerbated when the mechanisms underlying population dynamics are complex and depend on many parameters. In instances where non-parametric estimators of Ne such as the skyline struggle to reproduce the correct demographic history, model-based estimators which can draw on prior information about population size and growth rates may be more efficient. A coalescent model is developed for a large class of populations such that the demographic history is described by a deterministic nonlinear dynamical system of arbitrary dimension. This class of demographic model differs from those typically used in population genetics. Birth and death rates are not fixed, and no assumptions are made regarding the fraction of the population sampled. Furthermore, the population may be structured in such a way that gene copies reproduce both within and across demes. For this large class of models, it is shown how to derive the rate of coalescence, as well as the likelihood of a gene genealogy with heterochronous sampling and labeled taxa, and how to simulate a coalescent tree conditional on a complex demographic history. This theoretical framework encapsulates many of the models used by ecologists and epidemiologists and should facilitate the integration of population genetics with the study of mathematical population dynamics.},
	Author = {Volz, Erik McCullough},
	Copyright = {Copyright {\copyright} 2011, The Genetics Society of America},
	Date-Added = {2017-10-23 20:57:41 +0000},
	Date-Modified = {2017-10-23 20:57:41 +0000},
	Doi = {10.1534/genetics.111.134627},
	Issn = {0016-6731, 1943-2631},
	Journal = {Genetics},
	Keywords = {Coalescent, Infectious Disease, Mathematical Epidemiology, Population Genetics, Structured Populations},
	Language = {en},
	Month = jan,
	Pages = {genetics.111.134627},
	Pmid = {22042576},
	Title = {Complex {Population} {Dynamics} and the {Coalescent} under {Neutrality}},
	Url = {http://www.genetics.org/content/early/2011/10/27/genetics.111.134627},
	Urldate = {2017-10-23},
	Year = {2011},
	Bdsk-Url-1 = {http://www.genetics.org/content/early/2011/10/27/genetics.111.134627},
	Bdsk-Url-2 = {http://dx.doi.org/10.1534/genetics.111.134627}}

@article{mueller_mascot:_2017,
	Abstract = {{\textless}p{\textgreater}Motivation: The structured coalescent is widely applied to study demography within and migration between sub-populations from genetic sequence data. Current methods are either exact but too computationally inefficient to analyse large datasets with many states, or make strong approximations leading to severe biases in inference. We recently introduced an approximation based on weaker assumptions to the structured coalescent enabling the analysis of larger datasets with many different states. We showed that our approximation provides unbiased migration rate and population size estimates across a wide parameter range. Results: We here extend this approach by providing a new algorithm to calculate the probability of the state of internal nodes that includes the information from the full phylogenetic tree.We show that this algorithm is able to increase the probability attributed to the true node states. Furthermore we use improved integration techniques, such that our method is now able to analyse larger datasets, including a H3N2 dataset with 433 sequences sampled from 5 different locations. Availability: The here presented methods are combined into the BEAST2 package MASCOT, the Marginal Approximation of the Structured COalescenT. This package can be downloaded via the BEAUti package manager. The source code is available at https://github.com/nicfel/Mascot.git.{\textless}/p{\textgreater}},
	Author = {Mueller, Nicola Felix and Rasmussen, David Alan and Stadler, Tanja},
	Copyright = {{\copyright} 2017, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NonCommercial-NoDerivs 4.0 International), CC BY-NC-ND 4.0, as described at http://creativecommons.org/licenses/by-nc-nd/4.0/},
	Date-Added = {2017-10-23 20:51:35 +0000},
	Date-Modified = {2017-10-23 20:51:35 +0000},
	Doi = {10.1101/188516},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/F4VNIZBU/Mueller et al. - 2017 - MASCOT Parameter and state inference under the ma.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/GJKH2WNV/188516.html:text/html},
	Journal = {bioRxiv},
	Language = {en},
	Month = sep,
	Pages = {188516},
	Shorttitle = {{MASCOT}},
	Title = {{MASCOT}: {Parameter} and state inference under the marginal structured coalescent approximation},
	Url = {https://www.biorxiv.org/content/early/2017/09/13/188516},
	Urldate = {2017-10-23},
	Year = {2017},
	Bdsk-Url-1 = {https://www.biorxiv.org/content/early/2017/09/13/188516},
	Bdsk-Url-2 = {http://dx.doi.org/10.1101/188516}}

@article{carpenter_stan_2016,
	Author = {Carpenter, Bob and Gelman, Andrew and Hoffman, Matt and Lee, Daniel and Goodrich, Ben and Betancourt, Michael and Brubaker, Michael A and Guo, Jiqiang and Li, Peter and Riddell, Allen},
	Date-Added = {2017-08-06 23:18:56 +0000},
	Date-Modified = {2017-08-06 23:19:30 +0000},
	Journal = {J Stat Softw},
	Pages = {1--37},
	Title = {Stan: A probabilistic programming language},
	Volume = {20},
	Year = {2016}}

@article{adney_replication_2014,
	Abstract = {Camels infected with MERS-CoV show few symptoms and likely transmit the virus to humans and other camels through respiratory secretions., In 2012, a novel coronavirus associated with severe respiratory disease in humans emerged in the Middle East. Epidemiologic investigations identified dromedary camels as the likely source of zoonotic transmission of Middle East respiratory syndrome coronavirus (MERS-CoV). Here we provide experimental support for camels as a reservoir for MERS-CoV. We inoculated 3 adult camels with a human isolate of MERS-CoV and a transient, primarily upper respiratory tract infection developed in each of the 3 animals. Clinical signs of the MERS-CoV infection were benign, but each of the camels shed large quantities of virus from the upper respiratory tract. We detected infectious virus in nasal secretions through 7 days postinoculation, and viral RNA up to 35 days postinoculation. The pattern of shedding and propensity for the upper respiratory tract infection in dromedary camels may help explain the lack of systemic illness among naturally infected camels and the means of efficient camel-to-camel and camel-to-human transmission.},
	Author = {Adney, Danielle R. and van Doremalen, Neeltje and Brown, Vienna R. and Bushmaker, Trenton and Scott, Dana and de Wit, Emmie and Bowen, Richard A. and Munster, Vincent J.},
	Date-Added = {2017-08-05 20:09:36 +0000},
	Date-Modified = {2017-08-05 20:09:36 +0000},
	Doi = {10.3201/eid2012.141280},
	File = {PubMed Central Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/W39J4VMG/Adney et al. - 2014 - Replication and Shedding of MERS-CoV in Upper Resp.pdf:application/pdf},
	Issn = {1080-6040},
	Journal = {Emerging Infectious Diseases},
	Month = dec,
	Number = {12},
	Pages = {1999--2005},
	Pmcid = {PMC4257817},
	Pmid = {25418529},
	Title = {Replication and {Shedding} of {MERS}-{CoV} in {Upper} {Respiratory} {Tract} of {Inoculated} {Dromedary} {Camels}},
	Url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257817/},
	Volume = {20},
	Year = {2014},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257817/},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2012.141280}}

@article{volz_phylodynamics_2013,
	Author = {Volz, Erik M and Koelle, Katia and Bedford, Trevor},
	Date-Added = {2017-08-05 19:16:03 +0000},
	Date-Modified = {2017-08-05 19:16:22 +0000},
	Journal = {PLoS Comput Biol},
	Number = {3},
	Pages = {e1002947},
	Title = {Viral phylodynamics},
	Volume = {9},
	Year = {2013}}

@article{abdallah_camel_farming_2013,
	Author = {Abdallah, HR and Faye, Bernard},
	Date-Added = {2017-08-05 19:02:05 +0000},
	Date-Modified = {2017-08-05 19:02:31 +0000},
	Journal = {Emirates Journal of Food and Agriculture},
	Number = {4},
	Pages = {250},
	Title = {Typology of camel farming system in {Saudi Arabia}},
	Volume = {25},
	Year = {2013}}

@article{katoh_mafft_2013,
	Abstract = {We report a major update of the MAFFT multiple sequence alignment program. This version has several new features, including options for adding unaligned sequences into an existing alignment, adjustment of direction in nucleotide alignment, constrained alignment and parallel processing, which were implemented after the previous major update. This report shows actual examples to explain how these features work, alone and in combination. Some examples incorrectly aligned by MAFFT are also shown to clarify its limitations. We discuss how to avoid misalignments, and our ongoing efforts to overcome such limitations.},
	Author = {Katoh, Kazutaka and Standley, Daron M.},
	Date-Added = {2017-08-01 19:21:34 +0000},
	Date-Modified = {2017-08-01 19:21:34 +0000},
	Doi = {10.1093/molbev/mst010},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/AQ7FG3RI/Katoh and Standley - 2013 - MAFFT Multiple Sequence Alignment Software Version.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/76I4DQCV/MAFFT-Multiple-Sequence-Alignment-Software-Version.html:text/html},
	Issn = {0737-4038},
	Journal = {Molecular Biology and Evolution},
	Month = apr,
	Number = {4},
	Pages = {772--780},
	Shorttitle = {{MAFFT} {Multiple} {Sequence} {Alignment} {Software} {Version} 7},
	Title = {{MAFFT} {Multiple} {Sequence} {Alignment} {Software} {Version} 7: {Improvements} in {Performance} and {Usability}},
	Url = {https://academic.oup.com/mbe/article/30/4/772/1073398/MAFFT-Multiple-Sequence-Alignment-Software-Version},
	Urldate = {2017-08-01},
	Volume = {30},
	Year = {2013},
	Bdsk-Url-1 = {https://academic.oup.com/mbe/article/30/4/772/1073398/MAFFT-Multiple-Sequence-Alignment-Software-Version},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/mst010}}

@article{quick_rapid_2015,
	Abstract = {Foodborne outbreaks of Salmonella remain a pressing public health concern. We recently detected a large outbreak of Salmonella enterica serovar Enteritidis phage type 14b affecting more than 30 patients in our hospital. This outbreak was linked to community, national and European-wide cases. Hospital patients with Salmonella are at high risk, and require a rapid response. We initially investigated this outbreak by whole-genome sequencing using a novel rapid protocol on the Illumina MiSeq; we then integrated these data with whole-genome data from surveillance sequencing, thereby placing the outbreak in a national context. Additionally, we investigated the potential of a newly released sequencing technology, the MinION from Oxford Nanopore Technologies, in the management of a hospital outbreak of Salmonella.},
	Annote = {Pages 114 in PDF},
	Author = {Quick, Joshua and Ashton, Philip and Calus, Szymon and Chatt, Carole and Gossain, Savita and Hawker, Jeremy and Nair, Satheesh and Neal, Keith and Nye, Kathy and Peters, Tansy and De Pinna, Elizabeth and Robinson, Esther and Struthers, Keith and Webber, Mark and Catto, Andrew and Dallman, Timothy J. and Hawkey, Peter and Loman, Nicholas J.},
	Date-Added = {2017-07-31 20:50:58 +0000},
	Date-Modified = {2017-07-31 20:50:58 +0000},
	Doi = {10.1186/s13059-015-0677-2},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/PWZ4NW82/Quick et al. - 2015 - Rapid draft sequencing and real-time nanopore sequ.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/PUI8BIN5/s13059-015-0677-2.html:text/html},
	Issn = {1474-760X},
	Journal = {Genome Biology},
	Month = may,
	Pages = {114},
	Title = {Rapid draft sequencing and real-time nanopore sequencing in a hospital outbreak of {Salmonella}},
	Url = {https://doi.org/10.1186/s13059-015-0677-2},
	Volume = {16},
	Year = {2015},
	Bdsk-Url-1 = {https://doi.org/10.1186/s13059-015-0677-2},
	Bdsk-Url-2 = {http://dx.doi.org/10.1186/s13059-015-0677-2}}

@inproceedings{martinez_seasonality_2014,
	Author = {Martinez-Bakker, Micaela and Bakker, Kevin M and King, Aaron A and Rohani, Pejman},
	Booktitle = {Proc R Soc B},
	Date-Added = {2017-07-31 01:42:22 +0000},
	Date-Modified = {2017-07-31 01:42:45 +0000},
	Number = {1783},
	Pages = {20132438},
	Title = {Human birth seasonality: latitudinal gradient and interplay with childhood disease dynamics},
	Volume = {281},
	Year = {2014}}

@article{notohara_structured_coalescent_1990,
	Author = {Notohara, M},
	Date-Added = {2017-07-30 22:48:44 +0000},
	Date-Modified = {2017-07-30 22:49:14 +0000},
	Journal = {J Math Biol},
	Pages = {59--75},
	Title = {The coalescent and the genealogical process in geographically structured population},
	Volume = {29},
	Year = {1990}}

@article{lycett_h5n8_2016,
	Author = {Lycett, SJ and Bodewes, R and Pohlmann, A and Banks, J and Banyai, K and Boni, MF and Bouwstra, R and Breed, AC and Brown, IH and Chen, HL and others},
	Date-Added = {2017-07-30 22:40:46 +0000},
	Date-Modified = {2017-07-30 22:41:07 +0000},
	Journal = {Science},
	Number = {6309},
	Pages = {213--217},
	Title = {Role for migratory wild birds in the global spread of avian influenza {H5N8}},
	Volume = {354},
	Year = {2016}}

@article{liu_h7n9_2013,
	Author = {Liu, Di and Shi, Weifeng and Shi, Yi and Wang, Dayan and Xiao, Haixia and Li, Wei and Bi, Yuhai and Wu, Ying and Li, Xianbin and Yan, Jinghua and others},
	Date-Added = {2017-07-30 22:25:06 +0000},
	Date-Modified = {2017-07-30 22:25:58 +0000},
	Journal = {Lancet},
	Number = {9881},
	Pages = {1926--1932},
	Title = {Origin and diversity of novel avian influenza {A H7N9} viruses causing human infection: phylogenetic, structural, and coalescent analyses},
	Volume = {381},
	Year = {2013}}

@article{shinde_triple-reassortant_2009,
	Abstract = {Pigs have been hypothesized to act as a mixing vessel for the reassortment of avian, swine, and human influenza viruses and might play an important role in the emergence of novel influenza viruses capable of causing a human pandemic.1--3 Recent reports of widespread transmission of swine-origin influenza A (H1N1) viruses in humans in Mexico, the United States, and elsewhere highlight this ever-present threat to global public health.4,5 Between the 1930s and the 1990s, the most commonly circulating swine influenza virus among pigs --- classic swine influenza A (H1N1) --- underwent little change. However, by the late 1990s, multiple . . .},
	Author = {Shinde, Vivek and Bridges, Carolyn B. and Uyeki, Timothy M. and Shu, Bo and Balish, Amanda and Xu, Xiyan and Lindstrom, Stephen and Gubareva, Larisa V. and Deyde, Varough and Garten, Rebecca J. and Harris, Meghan and Gerber, Susan and Vagasky, Susan and Smith, Forrest and Pascoe, Neal and Martin, Karen and Dufficy, Deborah and Ritger, Kathy and Conover, Craig and Quinlisk, Patricia and Klimov, Alexander and Bresee, Joseph S. and Finelli, Lyn},
	Date-Added = {2017-07-26 22:39:55 +0000},
	Date-Modified = {2017-07-30 23:44:54 +0000},
	Journal = {N Engl J Med},
	Number = {25},
	Pages = {2616--2625},
	Title = {Triple-reassortant swine influenza {A (H1)} in humans in the {United States}, 2005--2009},
	Volume = {360},
	Year = {2009},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa0903812}}

@article{martinez_person--person_2005,
	Abstract = {Epidemiologic and genetic data show that person-to-person spread likely took place during the prodromal phase or shortly after it ended., Despite the fact that rodents are considered to be the infectious source of hantavirus for humans, another route of transmission was demonstrated. Andes virus (ANDV) has been responsible for most of the cases recorded in Argentina. Person-to-person transmission of ANDV Sout lineage was described during an outbreak of hantavirus pulmonary syndrome in southwest Argentina. In this study, we analyzed 4 clusters that occurred in 2 disease-endemic areas for different ANDV lineages. We found new evidence of interhuman transmission for ANDV Sout lineage and described the first event in which another lineage, ANDV Cent BsAs, was implicated in this mechanism of transmission. On the basis of epidemiologic and genetic data, we concluded that person-to-person spread of the virus likely took place during the prodromal phase or shortly after it ended, since close and prolonged contact occurred in the events analyzed here, and the incubation period was 15--24 days.},
	Author = {Martinez, Valeria P. and Bellomo, Carla and San Juan, Jorge and Pinna, Diego and Forlenza, Raul and Elder, Malco and Padula, Paula J.},
	Date-Added = {2017-07-26 22:31:46 +0000},
	Date-Modified = {2017-07-31 00:03:05 +0000},
	Journal = {Emerg Infect Dis},
	Number = {12},
	Pages = {1848--1853},
	Title = {Person-to-person transmission of {Andes} virus},
	Volume = {11},
	Year = {2005},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367635/},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid1112.050501}}

@article{reed_detection_2004,
	Abstract = {Monkeypox is an uncommon viral zoonosis caused by a member of the genus orthopoxvirus.1 Monkeypox was initially recognized in 1958 as a viral eruption of captive primates. The first cases in humans were reported in 1970 in Zaire (now the Democratic Republic of Congo).1 Since then, monkeypox has occurred sporadically in humans throughout that region2--9 but has not been reported outside Africa. During May and June 2003, an outbreak of febrile illness with skin eruptions occurred among residents of the midwestern United States.10 All patients reported having contact with sick pet prairie dogs (cynomys species) obtained through a common . . .},
	Author = {Reed, Kurt D. and Melski, John W. and Graham, Mary Beth and Regnery, Russell L. and Sotir, Mark J. and Wegner, Mark V. and Kazmierczak, James J. and Stratman, Erik J. and Li, Yu and Fairley, Janet A. and Swain, Geoffrey R. and Olson, Victoria A. and Sargent, Elizabeth K. and Kehl, Sue C. and Frace, Michael A. and Kline, Richard and Foldy, Seth L. and Davis, Jeffrey P. and Damon, Inger K.},
	Date-Added = {2017-07-26 22:17:45 +0000},
	Date-Modified = {2017-07-30 23:49:49 +0000},
	Journal = {N Engl J Med},
	Number = {4},
	Pages = {342--350},
	Title = {The detection of monkeypox in humans in the {Western Hemisphere}},
	Volume = {350},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa032299}}

@article{epperson_human_2013,
	Abstract = {Background. During August 2011--April 2012, 13 human infections with influenza A(H3N2) variant (H3N2v) virus were identified in the United States; 8 occurred in the prior 2 years. This virus differs from previous variant influenza viruses in that it contains the matrix (M) gene from the Influenza A(H1N1)pdm09 pandemic influenza virus.Methods. A case was defined as a person with laboratory-confirmed H3N2v virus infection. Cases and contacts were interviewed to determine exposure to swine and other animals and to assess potential person-to-person transmission.Results. Median age of cases was 4 years, and 12 of 13 (92\%) were children. Pig exposure was identified in 7 (54\%) cases. Six of 7 cases with swine exposure (86\%) touched pigs, and 1 (14\%) was close to pigs without known direct contact. Six cases had no swine exposure, including 2 clusters of suspected person-to-person transmission. All cases had fever; 12 (92\%) had respiratory symptoms, and 3 (23\%) were hospitalized for influenza. All 13 cases recovered.Conclusions. H3N2v virus infections were identified at a high rate from August 2011 to April 2012, and cases without swine exposure were identified in influenza-like illness outbreaks, indicating that limited person-to-person transmission likely occurred. Variant influenza viruses rarely result in sustained person-to-person transmission; however, the potential for this H3N2v virus to transmit efficiently is of concern. With minimal preexisting immunity in children and the limited cross-protective effect from seasonal influenza vaccine, the majority of children are susceptible to infection with this novel influenza virus.},
	Author = {Epperson, Scott and Jhung, Michael and Richards, Shawn and Quinlisk, Patricia and Ball, Lauren and Moll, M{\`a}ria and Boulton, Rachelle and Haddy, Loretta and Biggerstaff, Matthew and Brammer, Lynnette and Trock, Susan and Burns, Erin and Gomez, Thomas and Wong, Karen K. and Katz, Jackie and Lindstrom, Stephen and Klimov, Alexander and Bresee, Joseph S. and Jernigan, Daniel B. and Cox, Nancy and Finelli, Lyn},
	Date-Added = {2017-07-26 22:11:34 +0000},
	Date-Modified = {2017-07-31 00:04:15 +0000},
	Journal = {Clin Infect Dis},
	Number = {suppl\_1},
	Pages = {S4--S11},
	Title = {Human infections with influenza {A(H3N2)} variant virus in the {United States}, 2011--2012},
	Volume = {57},
	Year = {2013},
	Bdsk-Url-1 = {https://academic.oup.com/cid/article/57/suppl_1/S4/305385/Human-Infections-With-Influenza-A-H3N2-Variant},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/cid/cit272}}

@article{ladner_evolution_2015,
	Abstract = {The 2013--present Western African Ebola virus disease (EVD) outbreak is the largest ever recorded with {\textgreater}28,000 reported cases. Ebola virus (EBOV) genome sequencing has played an important role throughout this outbreak; however, relatively few sequences have been determined from patients in Liberia, the second worst-affected country. Here, we report 140 EBOV genome sequences from the second wave of the Liberian outbreak and analyze them in combination with 782 previously published sequences from throughout the Western African outbreak. While multiple early introductions of EBOV to Liberia are evident, the majority of Liberian EVD cases are consistent with a single introduction, followed by spread and diversification within the country. Movement of the virus within Liberia was widespread, and reintroductions from Liberia served as an important source for the continuation of the already ongoing EVD outbreak in Guinea. Overall, little evidence was found for incremental adaptation of EBOV to the human host.},
	Author = {Ladner, Jason T. and Wiley, Michael R. and Mate, Suzanne and Dudas, Gytis and Prieto, Karla and Lovett, Sean and Nagle, Elyse R. and Beitzel, Brett and Gilbert, Merle L. and Fakoli, Lawrence and Diclaro, Joseph W. and Schoepp, Randal J. and Fair, Joseph and Kuhn, Jens H. and Hensley, Lisa E. and Park, Daniel J. and Sabeti, Pardis C. and Rambaut, Andrew and Sanchez-Lockhart, Mariano and Bolay, Fatorma K. and Kugelman, Jeffrey R. and Palacios, Gustavo},
	Date-Added = {2017-07-11 19:02:21 +0000},
	Date-Modified = {2017-07-11 19:02:21 +0000},
	Doi = {10.1016/j.chom.2015.11.008},
	File = {ScienceDirect Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/7GSX5VI6/S193131281500462X.html:text/html},
	Issn = {1931-3128},
	Journal = {Cell Host \& Microbe},
	Month = dec,
	Number = {6},
	Pages = {659--669},
	Title = {Evolution and {Spread} of {Ebola} {Virus} in {Liberia}, 2014--2015},
	Url = {http://www.sciencedirect.com/science/article/pii/S193131281500462X},
	Volume = {18},
	Year = {2015},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S193131281500462X},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.chom.2015.11.008}}

@article{park_ebola_2015,
	Abstract = {The 2013--2015 Ebola virus disease (EVD) epidemic is caused by the Makona variant of Ebola virus (EBOV). Early in the epidemic, genome sequencing provided insights into virus evolution and transmission and offered important information for outbreak response. Here, we analyze sequences from 232 patients sampled over 7 months in Sierra Leone, along with 86 previously released genomes from earlier in the epidemic. We confirm sustained human-to-human transmission within Sierra Leone and find no evidence for import or export of EBOV across national borders after its initial introduction. Using high-depth replicate sequencing, we observe both host-to-host transmission and recurrent emergence of intrahost genetic variants. We trace the increasing impact of purifying selection in suppressing the accumulation of nonsynonymous mutations over time. Finally, we note changes in the mucin-like domain of EBOV glycoprotein that merit further investigation. These findings clarify the movement of EBOV within the region and describe viral evolution during prolonged human-to-human transmission.},
	Author = {Park, Daniel J. and Dudas, Gytis and Wohl, Shirlee and Goba, Augustine and Whitmer, Shannon L. M. and Andersen, Kristian G. and Sealfon, Rachel S. and Ladner, Jason T. and Kugelman, Jeffrey R. and Matranga, Christian B. and Winnicki, Sarah M. and Qu, James and Gire, Stephen K. and Gladden-Young, Adrianne and Jalloh, Simbirie and Nosamiefan, Dolo and Yozwiak, Nathan L. and Moses, Lina M. and Jiang, Pan-Pan and Lin, Aaron E. and Schaffner, Stephen F. and Bird, Brian and Towner, Jonathan and Mamoh, Mambu and Gbakie, Michael and Kanneh, Lansana and Kargbo, David and Massally, James L. B. and Kamara, Fatima K. and Konuwa, Edwin and Sellu, Josephine and Jalloh, Abdul A. and Mustapha, Ibrahim and Foday, Momoh and Yillah, Mohamed and Erickson, Bobbie R. and Sealy, Tara and Blau, Dianna and Paddock, Christopher and Brault, Aaron and Amman, Brian and Basile, Jane and Bearden, Scott and Belser, Jessica and Bergeron, Eric and Campbell, Shelley and Chakrabarti, Ayan and Dodd, Kimberly and Flint, Mike and Gibbons, Aridth and Goodman, Christin and Klena, John and McMullan, Laura and Morgan, Laura and Russell, Brandy and Salzer, Johanna and Sanchez, Angela and Wang, David and Jungreis, Irwin and Tomkins-Tinch, Christopher and Kislyuk, Andrey and Lin, Michael F. and Chapman, Sinead and MacInnis, Bronwyn and Matthews, Ashley and Bochicchio, James and Hensley, Lisa E. and Kuhn, Jens H. and Nusbaum, Chad and Schieffelin, John S. and Birren, Bruce W. and Forget, Marc and Nichol, Stuart T. and Palacios, Gustavo F. and Ndiaye, Daouda and Happi, Christian and Gevao, Sahr M. and Vandi, Mohamed A. and Kargbo, Brima and Holmes, Edward C. and Bedford, Trevor and Gnirke, Andreas and Str{\"o}her, Ute and Rambaut, Andrew and Garry, Robert F. and Sabeti, Pardis C.},
	Date-Added = {2017-07-11 19:01:46 +0000},
	Date-Modified = {2017-07-11 19:01:46 +0000},
	Doi = {10.1016/j.cell.2015.06.007},
	File = {ScienceDirect Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/3W2D3HQC/S009286741500690X.html:text/html},
	Issn = {0092-8674},
	Journal = {Cell},
	Month = jun,
	Number = {7},
	Pages = {1516--1526},
	Title = {Ebola {Virus} {Epidemiology}, {Transmission}, and {Evolution} during {Seven} {Months} in {Sierra} {Leone}},
	Url = {http://www.sciencedirect.com/science/article/pii/S009286741500690X},
	Volume = {161},
	Year = {2015},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S009286741500690X},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.cell.2015.06.007}}

@unpublished{who_mers_summary_2017,
	Abstract = {Middle East respiratory syndrome (MERS) is a viral respiratory disease caused by a novel coronavirus (MERS‐CoV) that was first identified in Saudi Arabia in 2012.},
	Author = {{World Health Organization}},
	Date-Added = {2017-07-10 22:40:03 +0000},
	Date-Modified = {2017-08-07 00:04:50 +0000},
	Note = {Available at http://www.who.int/emergencies/mers-cov/risk-assessment-july-2017.pdf},
	Title = {{WHO MERS-CoV} global summary and assessment of risk},
	Year = {2017},
	Bdsk-Url-1 = {http://www.who.int/mediacentre/factsheets/mers-cov/en/}}

@article{global_consortium_for_h5n8_and_related_influenza_viruses_role_2016,
	Abstract = {Avian influenza viruses affect both poultry production and public health. A subtype H5N8 (clade 2.3.4.4) virus, following an outbreak in poultry in South Korea in January 2014, rapidly spread worldwide in 2014-2015. Our analysis of H5N8 viral sequences, epidemiological investigations, waterfowl migration, and poultry trade showed that long-distance migratory birds can play a major role in the global spread of avian influenza viruses. Further, we found that the hemagglutinin of clade 2.3.4.4 virus was remarkably promiscuous, creating reassortants with multiple neuraminidase subtypes. Improving our understanding of the circumpolar circulation of avian influenza viruses in migratory waterfowl will help to provide early warning of threats from avian influenza to poultry, and potentially human, health.},
	Author = {{Global Consortium for H5N8 and Related Influenza Viruses}},
	Date-Added = {2017-07-10 18:41:37 +0000},
	Date-Modified = {2017-07-10 18:41:37 +0000},
	Doi = {10.1126/science.aaf8852},
	Issn = {1095-9203},
	Journal = {Science (New York, N.Y.)},
	Keywords = {Animal Migration, Animals, Birds, Disease Outbreaks, Europe, Hemagglutinins, Humans, Influenza A Virus, H5N8 Subtype, Influenza, Human, Influenza in Birds, Japan, Neuraminidase, North America, Phylogeography, Poultry, Reassortant Viruses, Republic of Korea},
	Language = {eng},
	Number = {6309},
	Pages = {213--217},
	Pmid = {27738169},
	Title = {Role for migratory wild birds in the global spread of avian influenza {H}5N8},
	Volume = {354},
	Year = {2016},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.aaf8852}}

@article{faria_simultaneously_2013,
	Abstract = {The factors that determine the origin and fate of cross-species transmission events remain unclear for the majority of human pathogens, despite being central for the development of predictive models and assessing the efficacy of prevention strategies. Here, we describe a flexible Bayesian statistical framework to reconstruct virus transmission between different host species based on viral gene sequences, while simultaneously testing and estimating the contribution of several potential predictors of cross-species transmission. Specifically, we use a generalized linear model extension of phylogenetic diffusion to perform Bayesian model averaging over candidate predictors. By further extending this model with branch partitioning, we allow for distinct host transition processes on external and internal branches, thus discriminating between recent cross-species transmissions, many of which are likely to result in dead-end infections, and host shifts that reflect successful onwards transmission in the new host species. Our approach corroborates genetic distance between hosts as a key determinant of both host shifts and cross-species transmissions of rabies virus in North American bats. Furthermore, our results indicate that geographical range overlap is a modest predictor for cross-species transmission, but not for host shifts. Although our evolutionary framework focused on the multi-host reservoir dynamics of bat rabies virus, it is applicable to other pathogens and to other discrete state transition processes.},
	Author = {Faria, Nuno Rodrigues and Suchard, Marc A. and Rambaut, Andrew and Streicker, Daniel G. and Lemey, Philippe},
	Date-Added = {2017-07-10 17:09:36 +0000},
	Date-Modified = {2017-07-30 22:44:10 +0000},
	Journal = {Phil Trans R Soc B},
	Pages = {20120196},
	Title = {Simultaneously reconstructing viral cross-species transmission history and identifying the underlying constraints},
	Volume = {368},
	Year = {2013},
	Bdsk-Url-1 = {http://rstb.royalsocietypublishing.org/content/368/1614/20120196},
	Bdsk-Url-2 = {http://dx.doi.org/10.1098/rstb.2012.0196}}

@article{herrewegh_1998,
	Abstract = {Recent evidence suggests that the type {II} feline coronavirus ({FCoV}) strains 79-1146 and 79-1683 have arisen from a homologous {RNA} recombination event between {FCoV} type I and canine coronavirus ({CCV}). In both cases, the template switch apparently took place between the S and M genes, giving rise to recombinant viruses which encode a {CCV}-like S protein and the M, N, 7a, and 7b proteins of {FCoV} type I (K. Motowaka, T. Hoh- datsu, H. Hashimoto, and H. Koyama, Microbiol. Immunol. 40:425--433, 1996; H. Vennema, A. Poland, K. Floyd Hawkins, and N. C. Pedersen, Feline Pract. 23:40--44, 1995). In the present study, we have looked for additional {FCoV}-{CCV} recombination sites. Four regions in the pol gene were selected for comparative sequence analysis of the type {II} {FCoV} strains 79-1683 and 79-1146, the type I {FCoV} strains {TN}406 and {UCD}1, the {CCV} strain K378, and the {TGEV} strain Purdue. Our data show that the type {II} {FCoVs} have arisen from double recombination events: additional crossover sites were mapped in the {ORF}1ab frameshifting region of strain 79-1683 and in the 5′ half of {ORF}1b of strain 79-1146.},
	Author = {Herrewegh, Arnold A. P. M. and Smeenk, Ingrid and Horzinek, Marian C. and Rottier, Peter J. M. and Groot, Raoul J. de},
	Date-Added = {2017-07-07 21:16:57 +0000},
	Date-Modified = {2017-07-30 23:59:12 +0000},
	Journal = {J Virol},
	Number = {5},
	Pages = {4508--4514},
	Title = {Feline Coronavirus Type {II} Strains 79-1683 and 79-1146 Originate from a Double Recombination between Feline Coronavirus Type {I} and Canine Coronavirus},
	Volume = {72},
	Year = {1998},
	Bdsk-Url-1 = {http://jvi.asm.org/content/72/5/4508}}

@article{kottier_1995,
	Abstract = {Embryonated eggs were coinfected with two strains of the coronavirus avian infectious bronchitis virus ({IBV}), {IBV}-Beaudette and {IBV}-M41, to investigate whether recombination between the two strains would occur. Virions were isolated from the allantoic fluid of the coinfected eggs and putative hybrid {RNAs} were detected by polymerase chain reaction ({PCR}), using strain-specific oligonucleotides. {PCR} products, of the expected sizes, were obtained as predicted from potential recombination events between the nucleoprotein (N) gene and the 3′-untranslated region of the two {IBV} genomes. Sequencing confirmed that they corresponded to hybrid {RNAs}. Virus produced as a result of the mixed infection was treated with an M41-specific neutralizing monoclonal antibody and passaged in Vero cells, in which {IBV}-Beaudette, but not {IBV}-M41, replicated. Hybrid {RNA} was still detectable after three serial passages. Since no {IBV}-M41 was detectable this confirmed that infectious recombinant genomes had been produced in the embryonated eggs. These findings not only support the circumstantial evidence, from sequencing studies of {IBV} field strains, that recombination occurs during replication of {IBV} and contributes to the diversity of {IBV}, but also show that coronavirus {RNA} recombination is not limited to mouse hepatitis virus.},
	Author = {Kottier, Sanneke A. and Cavanagh, David and Britton, Paul},
	Date-Added = {2017-07-07 21:16:49 +0000},
	Date-Modified = {2017-07-07 21:16:49 +0000},
	Doi = {10.1006/viro.1995.0029},
	File = {ScienceDirect Full Text PDF:/Users/admin/Library/Application Support/Firefox/Profiles/tit72ymn.default/zotero/storage/SUQDIUKA/KOTTIER et al. - 1995 - Experimental Evidence of Recombination in Coronavi.pdf:application/pdf;ScienceDirect Snapshot:/Users/admin/Library/Application Support/Firefox/Profiles/tit72ymn.default/zotero/storage/ZHNMQBIA/S0042682285700293.html:text/html},
	Issn = {0042-6822},
	Journal = {Virology},
	Month = nov,
	Number = {2},
	Pages = {569--580},
	Title = {Experimental Evidence of Recombination in Coronavirus Infectious Bronchitis Virus},
	Url = {http://www.sciencedirect.com/science/article/pii/S0042682285700293},
	Urldate = {2014-12-03},
	Volume = {213},
	Year = {1995},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S0042682285700293},
	Bdsk-Url-2 = {http://dx.doi.org/10.1006/viro.1995.0029}}

@article{keck_1988,
	Abstract = {{RNA}-{RNA} recombination between different strains of the murine coronavirus mouse hepatitis virus ({MHV}) occurs at a very high frequency in tissue culture. To demonstrate that {RNA} recombination may play a role in the evolution and pathogenesis of coronaviruses, we sought to determine whether {MHV} recombination could occur during replication in the animal host of the virus. By using two selectable markers, i.e., temperature sensitivity and monoclonal antibody neutralization, we isolated several recombinant viruses from the brains of mice infected with two different strains of {MHV}. The recombination frequency was very high, and recombination occurred at multiple sites on the viral {RNA} genome. This finding suggests that {RNA}-{RNA} recombination may play a significant role in natural evolution and neuropathogenesis of coronaviruses.},
	Author = {Keck, J G and Matsushima, G K and Makino, S and Fleming, J O and Vannier, D M and Stohlman, S A and Lai, M M},
	Date-Added = {2017-07-07 21:16:43 +0000},
	Date-Modified = {2017-07-30 23:56:08 +0000},
	Journal = {J Virol},
	Number = {5},
	Pages = {1810--1813},
	Title = {In vivo {RNA}-{RNA} recombination of coronavirus in mouse brain},
	Volume = {62},
	Year = {1988},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC253235/}}

@article{makino_1986,
	Abstract = {The {RNA} genome of coronaviruses consists of a single species of nonsegmented {RNA}. In this communication, we demonstrate that the {RNA} genomes of different strains of murine coronaviruses recombine during mixed infection at a very high frequency. Susceptible cells were coinfected with a temperature-sensitive mutant of one strain of mouse hepatitis virus ({MHV}) and a wild-type virus of a different strain. Of 21 randomly isolated viruses released from the coinfected cells at the nonpermissive temperature, 2 were recombinants which differed in the site of recombination. After three serial passages of the original virus pool derived from the mixed infection, the majority of the progeny viruses were recombinants. These recombinant viruses represented at least five different recombination sites between the two parental {MHV} strains. Such a high-frequency recombination between nonsegmented {RNA} genomes of {MHV} suggests that segmented {RNA} intermediates might be generated during {MHV} replication. We propose that the {RNA} replication of {MHV} proceeds in a discontinuous and nonprocessive manner, thus generating free segmented {RNA} intermediates, which could be used in {RNA} recombination via a copy-choice mechanism.},
	Author = {Makino, S. and Keck, J. G. and Stohlman, S. A. and Lai, M. M.},
	Date-Added = {2017-07-07 21:16:36 +0000},
	Date-Modified = {2017-07-30 23:54:45 +0000},
	Journal = {J Virol},
	Number = {3},
	Pages = {729--737},
	Title = {High-frequency {RNA} recombination of murine coronaviruses},
	Volume = {57},
	Year = {1986},
	Bdsk-Url-1 = {http://jvi.asm.org/content/57/3/729}}

@article{lai_1985,
	Abstract = {We have isolated a recombinant virus between the A59 and {JHM} strains of mouse hepatitis virus, which contain a single species of nonsegmented {RNA} genome. This recombinant was derived by mixed infection of {DBT} cells with temperature-sensitive mutants of A59 and {JHM} at nonpermissive temperature. Viruses recovered at this temperature were screened by oligonucleotide fingerprinting of their genomic {RNAs}. One recombinant virus, B1, was found to contain mostly A59-derived sequences, but the 3 kilobases at the 5' end of the genomic {RNA} was derived from {JHM}. Thus, the crossover point in the B1 genome is located within gene A, which codes for the viral {RNA} polymerases. The study of the intracellular {RNA} species of B1 virus revealed that probably all of the virus-specific subgenomic {mRNA} species contained the body sequences of strain A59 but the leader sequences of {JHM}. This result indicates that the {JHM} leader {RNA}, which differs from the A59 leader {RNA}, could be fused to the {mRNAs} of a different virus strain during {RNA} transcription. Furthermore, B1 virus-infected cells contain an additional subgenomic {mRNA} species which is transcribed from a new initiation site within gene C, suggesting that the leader {RNA} could determine the site of initiation for coronavirus {mRNAs}. These data represent a first report of {RNA} recombination between viruses, other than picornaviruses, which contain nonsegmented {RNA} genomes.},
	Author = {Lai, M. M. and Baric, R. S. and Makino, S. and Keck, J. G. and Egbert, J. and Leibowitz, J. L. and Stohlman, S. A.},
	Date-Added = {2017-07-07 21:16:02 +0000},
	Date-Modified = {2017-07-30 23:55:33 +0000},
	Journal = {J Virol},
	Number = {2},
	Pages = {449--456},
	Title = {Recombination between nonsegmented {RNA} genomes of murine coronaviruses},
	Volume = {56},
	Year = {1985},
	Bdsk-Url-1 = {http://jvi.asm.org/content/56/2/449}}

@article{chen_comparative_2017,
	Abstract = {MERS-CoV infection emerged in the Kingdom of Saudi Arabia (KSA) in 2012 and has spread to 26 countries. However, 80\% of all cases have occurred in KSA. The largest outbreak outside KSA occurred in South Korea (SK) in 2015. In this report, we describe an epidemiological comparison of the two outbreaks. Data from 1299 cases in KSA (2012--2015) and 186 cases in SK (2015) were collected from publicly available resources, including FluTrackers, the World Health Organization (WHO) outbreak news and the Saudi MOH (MOH). Descriptive analysis, t-tests, Chi-square tests and binary logistic regression were conducted to compare demographic and other characteristics (comorbidity, contact history) of cases by nationality. Epidemic curves of the outbreaks were generated. The mean age of cases was 51 years in KSA and 54 years in SK. Older males (70 years) were more likely to be infected or to die from MERS-CoV infection, and males exhibited increased rates of comorbidity in both countries. The epidemic pattern in KSA was more complex, with animal-to-human, human-to-human, nosocomial and unknown exposure, whereas the outbreak in SK was more clearly nosocomial. Of the 1186 MERS cases in KSA with reported risk factors, 158 (13.3\%) cases were hospital associated compared with 175 (94.1\%) in SK, and an increased proportion of cases with unknown exposure risk was found in KSA (710, 59.9\%). In a globally connected world, travel is a risk factor for emerging infections, and health systems in all countries should implement better triage systems for potential imported cases of MERS-CoV to prevent large epidemics.},
	Author = {Chen, Xin and Chughtai, Abrar Ahmad and Dyda, Amalie and MacIntyre, Chandini Raina},
	Date-Added = {2017-06-24 15:35:24 +0000},
	Date-Modified = {2017-07-31 00:10:44 +0000},
	Journal = {Emerg Microbes Infect},
	Number = {6},
	Pages = {e51},
	Title = {Comparative epidemiology of {Middle} {East} respiratory syndrome coronavirus ({MERS}-{CoV}) in {Saudi} {Arabia} and {South} {Korea}},
	Volume = {6},
	Year = {2017},
	Bdsk-Url-1 = {https://www.nature.com/emi/journal/v6/n6/full/emi201740a.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/emi.2017.40}}

@book{mersfactsheet,
	Author = {{World Health Organization}},
	Date-Added = {2017-06-20 05:00:00 +0000},
	Date-Modified = {2017-06-20 05:04:06 +0000},
	Publisher = {Available at \url{http://www.who.int/emergencies/mers-cov/en/}},
	Title = {{Middle East respiratory syndrome coronavirus (MERS-CoV)}},
	Year = {2017},
	Bdsk-Url-1 = {http://www.who.int/mediacentre/factsheets/fs211/en/}}

@article{bedford_strength_2011,
	Abstract = {RNA viruses evolve extremely quickly, allowing them to rapidly adapt to new environmental conditions. Viral pathogens, such as influenza virus, exploit this capacity for evolutionary change to persist within the human population despite substantial immune pressure. Understanding the process of adaptation in these viral systems is essential to our efforts to combat infectious disease.},
	Annote = {Pages 220 in PDF},
	Author = {Bedford, Trevor and Cobey, Sarah and Pascual, Mercedes},
	Date-Added = {2017-06-08 23:22:10 +0000},
	Date-Modified = {2017-07-31 00:21:38 +0000},
	Journal = {BMC Evol Biol},
	Pages = {220},
	Title = {Strength and tempo of selection revealed in viral gene genealogies},
	Volume = {11},
	Year = {2011},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-11-220}}

@article{pond_gard:_2006,
	Author = {Pond, Kosakovsky and L, Sergei and Posada, David and Gravenor, Michael B. and Woelk, Christopher H. and Frost, Simon D. W.},
	Date-Added = {2017-06-08 22:02:29 +0000},
	Date-Modified = {2017-06-08 22:02:29 +0000},
	Doi = {10.1093/bioinformatics/btl474},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/STZNAKFV/Pond et al. - 2006 - GARD a genetic algorithm for recombination detect.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/3MQ29Z8K/GARD-a-genetic-algorithm-for-recombination.html:text/html},
	Issn = {1367-4803},
	Journal = {Bioinformatics},
	Month = dec,
	Number = {24},
	Pages = {3096--3098},
	Shorttitle = {{GARD}},
	Title = {{GARD}: a genetic algorithm for recombination detection},
	Url = {https://academic.oup.com/bioinformatics/article/22/24/3096/208339/GARD-a-genetic-algorithm-for-recombination},
	Urldate = {2017-06-08},
	Volume = {22},
	Year = {2006},
	Bdsk-Url-1 = {https://academic.oup.com/bioinformatics/article/22/24/3096/208339/GARD-a-genetic-algorithm-for-recombination},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/bioinformatics/btl474}}

@article{hon_evidence_2008,
	Abstract = {Bats have been identified as the natural reservoir of severe acute respiratory syndrome (SARS)-like and SARS coronaviruses (SLCoV and SCoV). However, previous studies suggested that none of the currently sampled bat SLCoVs is the descendant of the direct ancestor of SCoV, based on their relatively distant phylogenetic relationship. In this study, evidence of the recombinant origin of the genome of a bat SLCoV is demonstrated. We identified a potential recombination breakpoint immediately after the consensus intergenic sequence between open reading frame 1 and the S coding region, suggesting the replication intermediates may participate in the recombination event, as previously speculated for other CoVs. Phylogenetic analysis of its parental regions suggests the presence of an uncharacterized SLCoV lineage that is phylogenetically closer to SCoVs than any of the currently sampled bat SLCoVs. Using various Bayesian molecular-clock models, interspecies transfer of this SLCoV lineage from bats to the amplifying host (e.g., civets) was estimated to have happened a median of 4.08 years before the SARS outbreak. Based on this relatively short window period, we speculate that this uncharacterized SLCoV lineage may contain the direct ancestor of SCoV. This study sheds light on the possible host bat species of the direct ancestor of SCoV, providing valuable information on the scope and focus of surveillance for the origin of SCoV.},
	Author = {Hon, Chung-Chau and Lam, Tsan-Yuk and Shi, Zheng-Li and Drummond, Alexei J. and Yip, Chi-Wai and Zeng, Fanya and Lam, Pui-Yi and Leung, Frederick Chi-Ching},
	Date-Added = {2017-06-08 21:58:43 +0000},
	Date-Modified = {2017-07-30 23:58:23 +0000},
	Journal = {J Virol},
	Number = {4},
	Pages = {1819--1826},
	Title = {Evidence of the recombinant origin of a bat severe acute respiratory syndrome ({SARS})-like coronavirus and its implications on the direct ancestor of {SARS} coronavirus},
	Volume = {82},
	Year = {2008},
	Bdsk-Url-1 = {http://jvi.asm.org/content/82/4/1819},
	Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.01926-07}}

@article{almutairi_non-genetic_2010,
	Abstract = {Reproductive traits and calving weight were assessed in Saudi camels, and non-genetic factors influencing them were studied using data collected at Al Jouf centre from 1987 to 2009. Age at first conce},
	Author = {Almutairi, Sallal E. and Boujenane, Isma{\"\i}l and Musaad, Abdelgader and Awad-Acharari, Falah},
	Date-Added = {2017-06-06 23:22:46 +0000},
	Date-Modified = {2017-07-31 00:24:17 +0000},
	Journal = {Trop Anim Health Prod},
	Number = {6},
	Pages = {1087--1092},
	Title = {Non-genetic factors influencing reproductive traits and calving weight in {Saudi} camels},
	Volume = {42},
	Year = {2010},
	Bdsk-Url-1 = {https://link.springer.com/article/10.1007/s11250-010-9529-y},
	Bdsk-Url-2 = {http://dx.doi.org/10.1007/s11250-010-9529-y}}

@article{wernery_camelid_2001,
	Abstract = {Camelid immunoglobulins differ from all other known antibodies and contradict all common theories on antibody diversity. It was demonstrated that up to 75 \% of all serum proteins are immunoglobulin G (IgG) molecules lacking light chains. IgG2 and IgG3, which only consist of heavy chains, have a low molecular weight which improves their biodistribution and allows a better tissue penetration. Of special importance is the long complementary determining region (CDR) loop which inserts deep into the active site of an enzyme. This binding property was only observed in experiments to gain structural data and to point out the extraordinary value of heavy chain antibodies as biochemical and pharmacological tools. The acquisition and absorption of adequate amounts of colostral immunoglobulins are essential to the health of the neonate. Pre-colostrum serum IgG levels in camelids are low, with concentrations of 0.26 $\pm$ 0.23 mg/ml. Maximum IgG levels are reached after 24 h and kept at a plateau with concentrations of 24.52 $\pm$ 8.8 mg/dl. IgG concentrations above 10 mg/ml indicate a successful passive transfer. IgG levels decline after 2--5 weeks and a marked increase is observed between 1 and 2 months, indicating that the immune system of the neonate has started to mature. A number of different tests are available for the assessment of IgG serum levels. Single radial immunodiffusion (SRID) is the only method that specifically measures serum IgG concentrations. It is a reliable assay to test failure of passive transfer (FPT). FPT is a major factor in neonatal mortality in camelids, but very little has been published so far. Therapeutic administration of colostrum will provide passive protection against infectious diseases for a 2--3-week period of risk, and the intravenous administration of 20--40 ml of camelid plasma helps to combat FPT.},
	Author = {Wernery, U.},
	Date-Added = {2017-06-06 23:00:41 +0000},
	Date-Modified = {2017-07-30 23:13:00 +0000},
	Journal = {J Vet Med B},
	Number = {8},
	Pages = {561--568},
	Title = {Camelid immunoglobulins and their importance for the new-born -- a review},
	Volume = {48},
	Year = {2001},
	Bdsk-Url-1 = {http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0450.2001.00478.x/abstract},
	Bdsk-Url-2 = {http://dx.doi.org/10.1111/j.1439-0450.2001.00478.x}}

@article{quick_real-time_2016,
	Abstract = {The Ebola virus disease epidemic in West Africa is the largest on record, responsible for over 28,599 cases and more than 11,299 deaths. Genome sequencing in viral outbreaks is desirable to characterize the infectious agent and determine its evolutionary rate. Genome sequencing also allows the identification of signatures of host adaptation, identification and monitoring of diagnostic targets, and characterization of responses to vaccines and treatments. The Ebola virus (EBOV) genome substitution rate in the Makona strain has been estimated at between 0.87 × 10−3 and 1.42 × 10−3 mutations per site per year. This is equivalent to 16--27 mutations in each genome, meaning that sequences diverge rapidly enough to identify distinct sub-lineages during a prolonged epidemic. Genome sequencing provides a high-resolution view of pathogen evolution and is increasingly sought after for outbreak surveillance. Sequence data may be used to guide control measures, but only if the results are generated quickly enough to inform interventions. Genomic surveillance during the epidemic has been sporadic owing to a lack of local sequencing capacity coupled with practical difficulties transporting samples to remote sequencing facilities. To address this problem, here we devise a genomic surveillance system that utilizes a novel nanopore DNA sequencing instrument. In April 2015 this system was transported in standard airline luggage to Guinea and used for real-time genomic surveillance of the ongoing epidemic. We present sequence data and analysis of 142 EBOV samples collected during the period March to October 2015. We were able to generate results less than 24 h after receiving an Ebola-positive sample, with the sequencing process taking as little as 15--60 min. We show that real-time genomic surveillance is possible in resource-limited settings and can be established rapidly to monitor outbreaks.},
	Author = {Quick, Joshua and Loman, Nicholas J. and Duraffour, Sophie and Simpson, Jared T. and Severi, Ettore and Cowley, Lauren and Bore, Joseph Akoi and Koundouno, Raymond and Dudas, Gytis and Mikhail, Amy and Ou{\'e}draogo, Nobila and Afrough, Babak and Bah, Amadou and Baum, Jonathan H. J. and Becker-Ziaja, Beate and Boettcher, Jan Peter and Cabeza-Cabrerizo, Mar and Camino-S{\'a}nchez, {\'A}lvaro and Carter, Lisa L. and Doerrbecker, Juliane and Enkirch, Theresa and Dorival, Isabel Garc{\'\i}a- and Hetzelt, Nicole and Hinzmann, Julia and Holm, Tobias and Kafetzopoulou, Liana Eleni and Koropogui, Michel and Kosgey, Abigael and Kuisma, Eeva and Logue, Christopher H. and Mazzarelli, Antonio and Meisel, Sarah and Mertens, Marc and Michel, Janine and Ngabo, Didier and Nitzsche, Katja and Pallasch, Elisa and Patrono, Livia Victoria and Portmann, Jasmine and Repits, Johanna Gabriella and Rickett, Natasha Y. and Sachse, Andreas and Singethan, Katrin and Vitoriano, In{\^e}s and Yemanaberhan, Rahel L. and Zekeng, Elsa G. and Racine, Trina and Bello, Alexander and Sall, Amadou Alpha and Faye, Ousmane and Faye, Oumar and Magassouba, N'Faly and Williams, Cecelia V. and Amburgey, Victoria and Winona, Linda and Davis, Emily and Gerlach, Jon and Washington, Frank and Monteil, Vanessa and Jourdain, Marine and Bererd, Marion and Camara, Alimou and Somlare, Hermann and Camara, Abdoulaye and Gerard, Marianne and Bado, Guillaume and Baillet, Bernard and Delaune, D{\'e}borah and Nebie, Koumpingnin Yacouba and Diarra, Abdoulaye and Savane, Yacouba and Pallawo, Raymond Bernard and Gutierrez, Giovanna Jaramillo and Milhano, Natacha and Roger, Isabelle and Williams, Christopher J. and Yattara, Facinet and Lewandowski, Kuiama and Taylor, James and Rachwal, Phillip and J. Turner, Daniel and Pollakis, Georgios and Hiscox, Julian A. and Matthews, David A. and Shea, Matthew K. O' and Johnston, Andrew McD and Wilson, Duncan and Hutley, Emma and Smit, Erasmus and Di Caro, Antonino and W{\"o}lfel, Roman and Stoecker, Kilian and Fleischmann, Erna and Gabriel, Martin and Weller, Simon A. and Koivogui, Lamine and Diallo, Boubacar and Ke{\"\i}ta, Sakoba and Rambaut, Andrew and Formenty, Pierre and G{\"u}nther, Stephan and Carroll, Miles W.},
	Copyright = {{\copyright} 2016 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
	Date-Added = {2017-06-06 22:30:15 +0000},
	Date-Modified = {2017-06-06 22:30:15 +0000},
	Doi = {10.1038/nature16996},
	File = {Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/DFNDZT2X/nature16996.html:text/html},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Microbial genetics, Microbiology, Molecular evolution, Next-generation sequencing, Viral infection},
	Language = {en},
	Month = feb,
	Number = {7589},
	Pages = {228--232},
	Title = {Real-time, portable genome sequencing for {Ebola} surveillance},
	Url = {http://www.nature.com/nature/journal/v530/n7589/abs/nature16996.html},
	Urldate = {2017-06-06},
	Volume = {530},
	Year = {2016},
	Bdsk-Url-1 = {http://www.nature.com/nature/journal/v530/n7589/abs/nature16996.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature16996}}

@article{ayres_beagle:_2012,
	Author = {Ayres, Daniel L. and Darling, Aaron and Zwickl, Derrick J. and Beerli, Peter and Holder, Mark T. and Lewis, Paul O. and Huelsenbeck, John P. and Ronquist, Fredrik and Swofford, David L. and Cummings, Michael P. and Rambaut, Andrew and Suchard, Marc A.},
	Date-Added = {2017-06-06 21:51:27 +0000},
	Date-Modified = {2017-06-20 05:17:00 +0000},
	Doi = {10.1093/sysbio/syr100},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/2DMSXGBC/Ayres et al. - 2012 - BEAGLE An Application Programming Interface and H.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/KCBRKE24/1680634.html:text/html},
	Issn = {1063-5157},
	Journal = {Syst Biol},
	Month = jan,
	Number = {1},
	Pages = {170--173},
	Shorttitle = {{BEAGLE}},
	Title = {{BEAGLE}: an application programming interface and high-performance computing library for statistical phylogenetics},
	Url = {https://academic.oup.com/sysbio/article/61/1/170/1680634/BEAGLE-An-Application-Programming-Interface-and},
	Urldate = {2017-06-06},
	Volume = {61},
	Year = {2012},
	Bdsk-Url-1 = {https://academic.oup.com/sysbio/article/61/1/170/1680634/BEAGLE-An-Application-Programming-Interface-and},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/sysbio/syr100}}

@article{maio_new_2015,
	Abstract = {Author Summary When studying infectious diseases it is often important to understand how germs spread from location-to-location, person-to-person, or even one part of the body to another. Using phylogeographic methods, it is possible to recover the history of spread of pathogens (or other organisms) by studying their genetic material. Here we reveal that some popular, fast phylogeographic methods are inaccurate, and we introduce a new more reliable method to address the problem. By comparing different phylogeographic methods based on principled population models and fast alternatives, we found that different approaches can give diametrically opposed results, and we offer concrete examples in the context of the ongoing Ebola outbreak in West Africa and the world-wide outbreaks of Avian Influenza Virus and Tomato Yellow Leaf Curl Virus. We found that the most popular phylogeographic method often produces completely inaccurate conclusions. One of the reasons for its popularity has been its computational speed, which has allowed users to analyse large genetic datasets with complex models. More accurate approaches have until now been considerably slower, and therefore we propose a new method called BASTA that achieves good accuracy in a reasonable time. We are relying more and more on genetic sequencing to learn about the origin and spread of infections, and as this role continues to grow, it will be essential to use accurate phylogeographic methods when designing policies to prevent or curb the spread of disease.},
	Author = {Maio, Nicola De and Wu, Chieh-Hsi and O'Reilly, Kathleen M. and Wilson, Daniel},
	Date-Added = {2017-06-06 21:49:18 +0000},
	Date-Modified = {2017-06-06 21:49:18 +0000},
	Doi = {10.1371/journal.pgen.1005421},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/H3S56WMZ/Maio et al. - 2015 - New Routes to Phylogeography A Bayesian Structure.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/PBVR58NJ/article.html:text/html},
	Issn = {1553-7404},
	Journal = {PLOS Genetics},
	Keywords = {a, b, C, D, e, f, G, h, i, l, m, n, o, p, r, s, t, u, v, y, z},
	Month = aug,
	Number = {8},
	Pages = {e1005421},
	Shorttitle = {New {Routes} to {Phylogeography}},
	Title = {New {Routes} to {Phylogeography}: {A} {Bayesian} {Structured} {Coalescent} {Approximation}},
	Url = {http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005421},
	Urldate = {2017-06-06},
	Volume = {11},
	Year = {2015},
	Bdsk-Url-1 = {http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005421},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pgen.1005421}}

@article{lloyd-smith_superspreading_2005,
	Abstract = {Population-level analyses often use average quantities to describe heterogeneous systems, particularly when variation does not arise from identifiable groups. A prominent example, central to our current understanding of epidemic spread, is the basic reproductive number, R0, which is defined as the mean number of infections caused by an infected individual in a susceptible population. Population estimates of R0 can obscure considerable individual variation in infectiousness, as highlighted during the global emergence of severe acute respiratory syndrome (SARS) by numerous 'superspreading events' in which certain individuals infected unusually large numbers of secondary cases. For diseases transmitted by non-sexual direct contacts, such as SARS or smallpox, individual variation is difficult to measure empirically, and thus its importance for outbreak dynamics has been unclear. Here we present an integrated theoretical and statistical analysis of the influence of individual variation in infectiousness on disease emergence. Using contact tracing data from eight directly transmitted diseases, we show that the distribution of individual infectiousness around R0 is often highly skewed. Model predictions accounting for this variation differ sharply from average-based approaches, with disease extinction more likely and outbreaks rarer but more explosive. Using these models, we explore implications for outbreak control, showing that individual-specific control measures outperform population-wide measures. Moreover, the dramatic improvements achieved through targeted control policies emphasize the need to identify predictive correlates of higher infectiousness. Our findings indicate that superspreading is a normal feature of disease spread, and to frame ongoing discussion we propose a rigorous definition for superspreading events and a method to predict their frequency.},
	Author = {Lloyd-Smith, J. O. and Schreiber, S. J. and Kopp, P. E. and Getz, W. M.},
	Copyright = {{\copyright} 2005 Nature Publishing Group},
	Date-Added = {2017-06-05 22:24:17 +0000},
	Date-Modified = {2017-06-05 22:24:17 +0000},
	Doi = {10.1038/nature04153},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/W6XDEWCS/Lloyd-Smith et al. - 2005 - Superspreading and the effect of individual variat.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/MNEHIV57/nature04153.html:text/html},
	Issn = {0028-0836},
	Journal = {Nature},
	Language = {en},
	Month = nov,
	Number = {7066},
	Pages = {355--359},
	Title = {Superspreading and the effect of individual variation on disease emergence},
	Url = {https://www.nature.com/nature/journal/v438/n7066/full/nature04153.html},
	Urldate = {2017-06-05},
	Volume = {438},
	Year = {2005},
	Bdsk-Url-1 = {https://www.nature.com/nature/journal/v438/n7066/full/nature04153.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature04153}}

@article{blumberg_inference_2013,
	Abstract = {Author Summary This paper focuses on infectious diseases such as monkeypox, Nipah virus and avian influenza that transmit weakly from human to human. These pathogens cannot cause self-sustaining epidemics in the human population, but instead cause limited transmission chains that stutter to extinction. Such pathogens would go extinct if they were confined to humans, but they persist because of continual introduction from an external reservoir (such as animals, for the zoonotic diseases mentioned above). They are important to study because they pose a risk of emerging if they become more transmissible, or conversely to monitor the success of efforts to locally eliminate a pathogen by vaccination. A crucial challenge for these `stuttering' pathogens is to quantify their transmissibility, in terms of the intensity and heterogeneity of disease transmission by infected individuals. In this paper, we use monkeypox as an example to show how these transmission properties can be estimated from commonly available data describing the size of observed stuttering chains. These results make it easier to monitor diseases that pose a risk of emerging (or re-emerging) as self-sustaining human pathogens, or to decide whether a seemingly large chain may signal a worrisome change in transmissibility.},
	Author = {Blumberg, Seth and Lloyd-Smith, James O.},
	Date-Added = {2017-06-05 22:20:34 +0000},
	Date-Modified = {2017-07-31 00:20:38 +0000},
	Journal = {PLoS Comput Biol},
	Number = {5},
	Pages = {e1002993},
	Title = {Inference of {$R_0$} and transmission heterogeneity from the size distribution of stuttering chains},
	Volume = {9},
	Year = {2013},
	Bdsk-Url-1 = {http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1002993},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pcbi.1002993}}

@article{boni_exact_2007,
	Abstract = {Statistical tests for detecting mosaic structure or recombination among nucleotide sequences usually rely on identifying a pattern or a signal that would be unlikely to appear under clonal reproduction. Dozens of such tests have been described, but many are hampered by long running times, confounding of selection and recombination, and/or inability to isolate the mosaic-producing event. We introduce a test that is exact, nonparametric, rapidly computable, free of the infinite-sites assumption, able to distinguish between recombination and variation in mutation/fixation rates, and able to identify the breakpoints and sequences involved in the mosaic-producing event. Our test considers three sequences at a time: two parent sequences that may have recombined, with one or two breakpoints, to form the third sequence (the child sequence). Excess similarity of the child sequence to a candidate recombinant of the parents is a sign of recombination; we take the maximum value of this excess similarity as our test statistic Δm,n,b. We present a method for rapidly calculating the distribution of Δm,n,b and demonstrate that it has comparable power to and a much improved running time over previous methods, especially in detecting recombination in large data sets.},
	Author = {Boni, Maciej F. and Posada, David and Feldman, Marcus W.},
	Date-Added = {2017-06-05 22:05:17 +0000},
	Date-Modified = {2017-07-31 00:16:20 +0000},
	Journal = {Genetics},
	Number = {2},
	Pages = {1035--1047},
	Title = {An exact nonparametric method for inferring mosaic structure in sequence triplets},
	Volume = {176},
	Year = {2007},
	Bdsk-Url-1 = {http://www.genetics.org/content/176/2/1035},
	Bdsk-Url-2 = {http://dx.doi.org/10.1534/genetics.106.068874}}

@article{bruen_simple_2006,
	Abstract = {Recombination is a powerful evolutionary force that merges historically distinct genotypes. But the extent of recombination within many organisms is unknown, and even determining its presence within a set of homologous sequences is a difficult question. Here we develop a new statistic, Φw, that can be used to test for recombination. We show through simulation that our test can discriminate effectively between the presence and absence of recombination, even in diverse situations such as exponential growth (star-like topologies) and patterns of substitution rate correlation. A number of other tests, Max χ2, NSS, a coalescent-based likelihood permutation test (from LDHat), and correlation of linkage disequilibrium (both r2 and {\textbar}D′{\textbar}) with distance, all tend to underestimate the presence of recombination under strong population growth. Moreover, both Max χ2 and NSS falsely infer the presence of recombination under a simple model of mutation rate correlation. Results on empirical data show that our test can be used to detect recombination between closely as well as distantly related samples, regardless of the suspected rate of recombination. The results suggest that Φw is one of the best approaches to distinguish recurrent mutation from recombination in a wide variety of circumstances.},
	Author = {Bruen, Trevor C. and Philippe, Herv{\'e} and Bryant, David},
	Date-Added = {2017-06-05 22:03:43 +0000},
	Date-Modified = {2017-07-31 00:12:08 +0000},
	Journal = {Genetics},
	Number = {4},
	Pages = {2665--2681},
	Title = {A simple and robust statistical test for detecting the presence of recombination},
	Volume = {172},
	Year = {2006},
	Bdsk-Url-1 = {http://www.genetics.org/content/172/4/2665},
	Bdsk-Url-2 = {http://dx.doi.org/10.1534/genetics.105.048975}}

@article{vijaykrishna_long-term_2011,
	Abstract = {Swine influenza A viruses (SwIV) cause significant economic losses in animal husbandry as well as instances of human disease and occasionally give rise to human pandemics, including that caused by the H1N1/2009 virus. The lack of systematic and longitudinal influenza surveillance in pigs has hampered attempts to reconstruct the origins of this pandemic. Most existing swine data were derived from opportunistic samples collected from diseased pigs in disparate geographical regions, not from prospective studies in defined locations, hence the evolutionary and transmission dynamics of SwIV are poorly understood. Here we quantify the epidemiological, genetic and antigenic dynamics of SwIV in Hong Kong using a data set of more than 650 SwIV isolates and more than 800 swine sera from 12 years of systematic surveillance in this region, supplemented with data stretching back 34 years. Intercontinental virus movement has led to reassortment and lineage replacement, creating an antigenically and genetically diverse virus population whose dynamics are quantitatively different from those previously observed for human influenza viruses. Our findings indicate that increased antigenic drift is associated with reassortment events and offer insights into the emergence of influenza viruses with epidemic potential in swine and humans.},
	Author = {Vijaykrishna, Dhanasekaran and Smith, Gavin J. D. and Pybus, Oliver G. and Zhu, Huachen and Bhatt, Samir and Poon, Leo L. M. and Riley, Steven and Bahl, Justin and Ma, Siu K. and Cheung, Chung L. and Perera, Ranawaka A. P. M. and Chen, Honglin and Shortridge, Kennedy F. and Webby, Richard J. and Webster, Robert G. and Guan, Yi and Peiris, J. S. Malik},
	Copyright = {{\copyright} 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
	Date-Added = {2017-06-05 22:01:34 +0000},
	Date-Modified = {2017-06-05 22:01:34 +0000},
	Doi = {10.1038/nature10004},
	File = {Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/U8CS6SI7/nature10004.html:text/html},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Ecology, Evolution, Genetics and genomics, Virology},
	Language = {en},
	Month = may,
	Number = {7348},
	Pages = {519--522},
	Title = {Long-term evolution and transmission dynamics of swine influenza {A} virus},
	Url = {http://www.nature.com/nature/journal/v473/n7348/full/nature10004.html},
	Urldate = {2017-06-05},
	Volume = {473},
	Year = {2011},
	Bdsk-Url-1 = {http://www.nature.com/nature/journal/v473/n7348/full/nature10004.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature10004}}

@article{ali_systematic_2017,
	Abstract = {Middle East respiratory syndrome coronavirus (MERS-CoV) causes severe human infections and dromedary camels are considered an intermediary host. The dynamics of natural infection in camels are not well understood. Through systematic surveillance in Egypt, nasal, rectal, milk, urine and serum samples were collected from camels between June 2014 and February 2016. Locations included quarantines, markets, abattoirs, free-roaming herds and farmed breeding herds. The overall seroprevalence was 71\% and RNA detection rate was 15\%. Imported camels had higher seroprevalence (90\% vs 61\%) and higher RT-PCR detection rates (21\% vs 12\%) than locally raised camels. Juveniles had lower seroprevalence than adults (37\% vs 82\%) but similar RT-PCR detection rates (16\% vs 15\%). An outbreak in a breeding herd, showed that antibodies rapidly wane, that camels become re-infected, and that outbreaks in a herd are sustained for an extended time. Maternal antibodies titers were very low in calves regardless of the antibody titers of the mothers. Our results support the hypothesis that camels are a reservoir for MERS-CoV and that camel trade is an important route of introducing the virus into importing countries. Findings related to waning antibodies and re-infection have implications for camel vaccine development, disease management and zoonotic threat.},
	Author = {Ali, Mohamed A. and Shehata, Mahmoud M. and Gomaa, Mokhtar R. and Kandeil, Ahmed and El-Shesheny, Rabeh and Kayed, Ahmed S. and El-Taweel, Ahmed N. and Atea, Mohamed and Hassan, Nagla and Bagato, Ola and Moatasim, Yassmin and Mahmoud, Sara H. and Kutkat, Omnia and Maatouq, Asmaa M. and Osman, Ahmed and McKenzie, Pamela P. and Webby, Richard J. and Kayali, Ghazi},
	Date-Added = {2017-06-05 21:54:47 +0000},
	Date-Modified = {2017-07-31 00:24:41 +0000},
	Journal = {Emerg Microbes Infect},
	Number = {1},
	Pages = {e1},
	Title = {Systematic, active surveillance for {Middle} {East} respiratory syndrome coronavirus in camels in {Egypt}},
	Volume = {6},
	Year = {2017},
	Bdsk-Url-1 = {http://www.nature.com/emi/journal/v6/n1/full/emi2016130a.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/emi.2016.130}}

@article{bedford_global_2015,
	Abstract = {Understanding the spatiotemporal patterns of emergence and circulation of new human seasonal influenza virus variants is a key scientific and public health challenge. The global circulation patterns of influenza A/H3N2 viruses are well characterized, but the patterns of A/H1N1 and B viruses have remained largely unexplored. Here we show that the global circulation patterns of A/H1N1 (up to 2009), B/Victoria, and B/Yamagata viruses differ substantially from those of A/H3N2 viruses, on the basis of analyses of 9,604 haemagglutinin sequences of human seasonal influenza viruses from 2000 to 2012. Whereas genetic variants of A/H3N2 viruses did not persist locally between epidemics and were reseeded from East and Southeast Asia, genetic variants of A/H1N1 and B viruses persisted across several seasons and exhibited complex global dynamics with East and Southeast Asia playing a limited role in disseminating new variants. The less frequent global movement of influenza A/H1N1 and B viruses coincided with slower rates of antigenic evolution, lower ages of infection, and smaller, less frequent epidemics compared to A/H3N2 viruses. Detailed epidemic models support differences in age of infection, combined with the less frequent travel of children, as probable drivers of the differences in the patterns of global circulation, suggesting a complex interaction between virus evolution, epidemiology, and human behaviour.},
	Author = {Bedford, Trevor and Riley, Steven and Barr, Ian G. and Broor, Shobha and Chadha, Mandeep and Cox, Nancy J. and Daniels, Rodney S. and Gunasekaran, C. Palani and Hurt, Aeron C. and Kelso, Anne and Klimov, Alexander and Lewis, Nicola S. and Li, Xiyan and McCauley, John W. and Odagiri, Takato and Potdar, Varsha and Rambaut, Andrew and Shu, Yuelong and Skepner, Eugene and Smith, Derek J. and Suchard, Marc A. and Tashiro, Masato and Wang, Dayan and Xu, Xiyan and Lemey, Philippe and Russell, Colin A.},
	Copyright = {{\copyright} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
	Date-Added = {2017-06-05 20:48:14 +0000},
	Date-Modified = {2017-06-05 20:48:14 +0000},
	Doi = {10.1038/nature14460},
	File = {Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/TSW4JAWB/nature14460.html:text/html},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Computational models, Data integration, Influenza virus, Phylogenetics},
	Language = {en},
	Month = jul,
	Number = {7559},
	Pages = {217--220},
	Title = {Global circulation patterns of seasonal influenza viruses vary with antigenic drift},
	Url = {http://www.nature.com/nature/journal/v523/n7559/abs/nature14460.html},
	Urldate = {2017-06-05},
	Volume = {523},
	Year = {2015},
	Bdsk-Url-1 = {http://www.nature.com/nature/journal/v523/n7559/abs/nature14460.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature14460}}

@article{dudas_virus_2017,
	Abstract = {The 2013--2016 West African epidemic caused by the Ebola virus was of unprecedented magnitude, duration and impact. Here we reconstruct the dispersal, proliferation and decline of Ebola virus throughout the region by analysing 1,610 Ebola virus genomes, which represent over 5\% of the known cases. We test the association of geography, climate and demography with viral movement among administrative regions, inferring a classic `gravity' model, with intense dispersal between larger and closer populations. Despite attenuation of international dispersal after border closures, cross-border transmission had already sown the seeds for an international epidemic, rendering these measures ineffective at curbing the epidemic. We address why the epidemic did not spread into neighbouring countries, showing that these countries were susceptible to substantial outbreaks but at lower risk of introductions. Finally, we reveal that this large epidemic was a heterogeneous and spatially dissociated collection of transmission clusters of varying size, duration and connectivity. These insights will help to inform interventions in future epidemics.
View full text},
	Author = {Dudas, Gytis and Carvalho, Luiz Max and Bedford, Trevor and Tatem, Andrew J. and Baele, Guy and Faria, Nuno R. and Park, Daniel J. and Ladner, Jason T. and Arias, Armando and Asogun, Danny and Bielejec, Filip and Caddy, Sarah L. and Cotten, Matthew and D'Ambrozio, Jonathan and Dellicour, Simon and Di Caro, Antonino and Diclaro, Joseph W. and Duraffour, Sophie and Elmore, Michael J. and Fakoli, Lawrence S. and Faye, Ousmane and Gilbert, Merle L. and Gevao, Sahr M. and Gire, Stephen and Gladden-Young, Adrianne and Gnirke, Andreas and Goba, Augustine and Grant, Donald S. and Haagmans, Bart L. and Hiscox, Julian A. and Jah, Umaru and Kugelman, Jeffrey R. and Liu, Di and Lu, Jia and Malboeuf, Christine M. and Mate, Suzanne and Matthews, David A. and Matranga, Christian B. and Meredith, Luke W. and Qu, James and Quick, Joshua and Pas, Suzan D. and Phan, My V. T. and Pollakis, Georgios and Reusken, Chantal B. and Sanchez-Lockhart, Mariano and Schaffner, Stephen F. and Schieffelin, John S. and Sealfon, Rachel S. and Simon-Loriere, Etienne and Smits, Saskia L. and Stoecker, Kilian and Thorne, Lucy and Tobin, Ekaete Alice and Vandi, Mohamed A. and Watson, Simon J. and West, Kendra and Whitmer, Shannon and Wiley, Michael R. and Winnicki, Sarah M. and Wohl, Shirlee and W{\"o}lfel, Roman and Yozwiak, Nathan L. and Andersen, Kristian G. and Blyden, Sylvia O. and Bolay, Fatorma and Carroll, Miles W. and Dahn, Bernice and Diallo, Boubacar and Formenty, Pierre and Fraser, Christophe and Gao, George F. and Garry, Robert F. and Goodfellow, Ian and G{\"u}nther, Stephan and Happi, Christian T. and Holmes, Edward C. and Kargbo, Brima and Ke{\"\i}ta, Sakoba and Kellam, Paul and Koopmans, Marion P. G. and Kuhn, Jens H. and Loman, Nicholas J. and Magassouba, N'Faly and Naidoo, Dhamari and Nichol, Stuart T. and Nyenswah, Tolbert and Palacios, Gustavo and Pybus, Oliver G. and Sabeti, Pardis C. and Sall, Amadou and Str{\"o}her, Ute and Wurie, Isatta and Suchard, Marc A. and Lemey, Philippe and Rambaut, Andrew},
	Copyright = {{\copyright} 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.},
	Date-Added = {2017-06-05 19:16:31 +0000},
	Date-Modified = {2017-06-05 19:16:31 +0000},
	Doi = {10.1038/nature22040},
	File = {Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/TBP62AH3/nature22040.html:text/html},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Epidemiology, Phylogenetics, Statistical methods, Viral infection},
	Language = {en},
	Month = apr,
	Number = {7650},
	Pages = {309--315},
	Title = {Virus genomes reveal factors that spread and sustained the {Ebola} epidemic},
	Url = {https://www.nature.com/nature/journal/v544/n7650/abs/nature22040.html},
	Urldate = {2017-06-05},
	Volume = {544},
	Year = {2017},
	Bdsk-Url-1 = {https://www.nature.com/nature/journal/v544/n7650/abs/nature22040.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature22040}}

@article{smith_dating_2009,
	Abstract = {Pandemic influenza viruses cause significant mortality in humans. In the 20th century, 3 influenza viruses caused major pandemics: the 1918 H1N1 virus, the 1957 H2N2 virus, and the 1968 H3N2 virus. These pandemics were initiated by the introduction and successful adaptation of a novel hemagglutinin subtype to humans from an animal source, resulting in antigenic shift. Despite global concern regarding a new pandemic influenza, the emergence pathway of pandemic strains remains unknown. Here we estimated the evolutionary history and inferred date of introduction to humans of each of the genes for all 20th century pandemic influenza strains. Our results indicate that genetic components of the 1918 H1N1 pandemic virus circulated in mammalian hosts, i.e., swine and humans, as early as 1911 and was not likely to be a recently introduced avian virus. Phylogenetic relationships suggest that the A/Brevig Mission/1/1918 virus (BM/1918) was generated by reassortment between mammalian viruses and a previously circulating human strain, either in swine or, possibly, in humans. Furthermore, seasonal and classic swine H1N1 viruses were not derived directly from BM/1918, but their precursors co-circulated during the pandemic. Mean estimates of the time of most recent common ancestor also suggest that the H2N2 and H3N2 pandemic strains may have been generated through reassortment events in unknown mammalian hosts and involved multiple avian viruses preceding pandemic recognition. The possible generation of pandemic strains through a series of reassortment events in mammals over a period of years before pandemic recognition suggests that appropriate surveillance strategies for detection of precursor viruses may abort future pandemics.},
	Author = {Smith, Gavin J. D. and Bahl, Justin and Vijaykrishna, Dhanasekaran and Zhang, Jinxia and Poon, Leo L. M. and Chen, Honglin and Webster, Robert G. and Peiris, J. S. Malik and Guan, Yi},
	Date-Added = {2017-06-05 19:14:37 +0000},
	Date-Modified = {2017-07-30 23:14:54 +0000},
	Journal = {Proc Natl Acad Sci USA},
	Number = {28},
	Pages = {11709--11712},
	Title = {Dating the emergence of pandemic influenza viruses},
	Volume = {106},
	Year = {2009},
	Bdsk-Url-1 = {http://www.pnas.org/content/106/28/11709},
	Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.0904991106}}

@article{turner_genomic_2005,
	Abstract = {Using DNA microarrays, the authors identify 3 small regions of the genome that differ between two forms of hybridizing mosquitoes; regions that are likely to contain the genes responsible for reproductive isolation.},
	Author = {Turner, Thomas L. and Hahn, Matthew W. and Nuzhdin, Sergey V.},
	Date-Added = {2017-06-05 19:01:24 +0000},
	Date-Modified = {2017-07-30 23:14:05 +0000},
	Journal = {PLoS Biol},
	Number = {9},
	Pages = {e285},
	Title = {Genomic islands of speciation in {Anopheles} gambiae},
	Volume = {3},
	Year = {2005},
	Bdsk-Url-1 = {http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0030285},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pbio.0030285}}

@article{dudas_reassortment_2015,
	Author = {Dudas, Gytis and Bedford, Trevor and Lycett, Samantha and Rambaut, Andrew},
	Date-Added = {2017-06-05 18:59:00 +0000},
	Date-Modified = {2017-07-31 00:06:51 +0000},
	Journal = {Mol Biol Evol},
	Number = {1},
	Pages = {162--172},
	Title = {Reassortment between influenza {B} lineages and the emergence of a coadapted {PB}1--{PB}2--{HA} gene complex},
	Volume = {32},
	Year = {2015},
	Bdsk-Url-1 = {https://academic.oup.com/mbe/article/32/1/162/2925578/Reassortment-between-Influenza-B-Lineages-and-the},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msu287}}

@article{drummond_bayesian_2012,
	Author = {Drummond, Alexei J. and Suchard, Marc A. and Xie, Dong and Rambaut, Andrew},
	Date-Added = {2017-05-10 21:43:54 +0000},
	Date-Modified = {2017-07-31 00:15:09 +0000},
	Journal = {Mol Biol Evol},
	Number = {8},
	Pages = {1969--1973},
	Title = {Bayesian phylogenetics with {BEAUti} and the {BEAST} 1.7},
	Volume = {29},
	Year = {2012},
	Bdsk-Url-1 = {https://academic.oup.com/mbe/article/29/8/1969/1044583/Bayesian-Phylogenetics-with-BEAUti-and-the-BEAST-1},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/mss075}}

@article{gill_2013,
	Author = {Gill, Mandev S. and Lemey, Philippe and Faria, Nuno R. and Rambaut, Andrew and Shapiro, Beth and Suchard, Marc A.},
	Date-Added = {2017-05-05 22:36:53 +0000},
	Date-Modified = {2017-07-31 00:00:20 +0000},
	Journal = {Mol Biol Evol},
	Number = {3},
	Pages = {713},
	Title = {Improving Bayesian Population Dynamics Inference: A Coalescent-Based Model for Multiple Loci},
	Volume = {30},
	Year = {2013},
	Bdsk-Url-1 = {+%20http://dx.doi.org/10.1093/molbev/mss265},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/mss265}}

@article{cauchemez_unraveling_2016,
	Abstract = {With more than 1,700 laboratory-confirmed infections, Middle East respiratory syndrome coronavirus (MERS-CoV) remains a significant threat for public health. However, the lack of detailed data on modes of transmission from the animal reservoir and between humans means that the drivers of MERS-CoV epidemics remain poorly characterized. Here, we develop a statistical framework to provide a comprehensive analysis of the transmission patterns underlying the 681 MERS-CoV cases detected in the Kingdom of Saudi Arabia (KSA) between January 2013 and July 2014. We assess how infections from the animal reservoir, the different levels of mixing, and heterogeneities in transmission have contributed to the buildup of MERS-CoV epidemics in KSA. We estimate that 12\% [95\% credible interval (CI): 9\%, 15\%] of cases were infected from the reservoir, the rest via human-to-human transmission in clusters (60\%; CI: 57\%, 63\%), within (23\%; CI: 20\%, 27\%), or between (5\%; CI: 2\%, 8\%) regions. The reproduction number at the start of a cluster was 0.45 (CI: 0.33, 0.58) on average, but with large SD (0.53; CI: 0.35, 0.78). It was {\textgreater}1 in 12\% (CI: 6\%, 18\%) of clusters but fell by approximately one-half (47\% CI: 34\%, 63\%) its original value after 10 cases on average. The ongoing exposure of humans to MERS-CoV from the reservoir is of major concern, given the continued risk of substantial outbreaks in health care systems. The approach we present allows the study of infectious disease transmission when data linking cases to each other remain limited and uncertain.},
	Author = {Cauchemez, Simon and Nouvellet, Pierre and Cori, Anne and Jombart, Thibaut and Garske, Tini and Clapham, Hannah and Moore, Sean and Mills, Harriet Linden and Salje, Henrik and Collins, Caitlin and Rodriquez-Barraquer, Isabel and Riley, Steven and Truelove, Shaun and Algarni, Homoud and Alhakeem, Rafat and AlHarbi, Khalid and Turkistani, Abdulhafiz and Aguas, Ricardo J. and Cummings, Derek A. T. and Kerkhove, Maria D. Van and Donnelly, Christl A. and Lessler, Justin and Fraser, Christophe and Al-Barrak, Ali and Ferguson, Neil M.},
	Date-Added = {2017-04-06 21:09:23 +0000},
	Date-Modified = {2017-07-31 00:11:15 +0000},
	Journal = {Proc Natl Acad Sci USA},
	Number = {32},
	Pages = {9081--9086},
	Title = {Unraveling the drivers of {MERS}-{CoV} transmission},
	Volume = {113},
	Year = {2016},
	Bdsk-Url-1 = {http://www.pnas.org/content/113/32/9081},
	Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.1519235113}}

@article{zhang_evolutionary_2016,
	Abstract = {Middle East respiratory syndrome coronavirus (MERS-CoV) belongs to beta group of coronavirus and was first discovered in 2012. MERS-CoV can infect multiple host species and cause severe diseases in human.},
	Author = {Zhang, Zhao and Shen, Libing and Gu, Xun},
	Date-Added = {2017-03-23 22:34:19 +0000},
	Date-Modified = {2017-07-30 23:07:20 +0000},
	Journal = {Sci Rep},
	Pages = {25049},
	Title = {Evolutionary dynamics of {MERS}-{CoV}: potential recombination, positive selection and transmission},
	Volume = {6},
	Year = {2016},
	Bdsk-Url-1 = {http://www.nature.com/srep/2016/160504/srep25049/full/srep25049.html},
	Bdsk-Url-2 = {http://dx.doi.org/10.1038/srep25049}}

@article{drummond_2006,
	Abstract = {This new method can simultaneously infer phylogeny and estimate the molecular clock. The
authors run their method on several large alignments to show its phylogenetic accuracy and
ability to infer a timescale to evolution.},
	Author = {Drummond, Alexei J and Ho, Simon Y. W and Phillips, Matthew J and Rambaut, Andrew},
	Date-Added = {2017-03-21 18:53:21 +0000},
	Date-Modified = {2017-03-21 18:53:21 +0000},
	Doi = {10.1371/journal.pbio.0040088},
	File = {PLoS Full Text PDF:/Users/admin/Library/Application Support/Firefox/Profiles/tit72ymn.default/zotero/storage/5ZKKU4F6/Drummond et al. - 2006 - Relaxed Phylogenetics and Dating with Confidence.pdf:application/pdf;PLoS Snapshot:/Users/admin/Library/Application Support/Firefox/Profiles/tit72ymn.default/zotero/storage/FDTSS3JR/journal.pbio.html:text/html},
	Journal = {{PLoS} Biol},
	Month = mar,
	Number = {5},
	Pages = {e88},
	Title = {Relaxed Phylogenetics and Dating with Confidence},
	Url = {http://dx.doi.org/10.1371/journal.pbio.0040088},
	Urldate = {2014-02-27},
	Volume = {4},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0040088}}

@article{hky_1985,
	Abstract = {A new statistical method for estimating divergence dates of species from {DNA} sequence data by a molecular clock approach is developed. This method takes into account effectively the information contained in a set of {DNA} sequence data. The molecular clock of mitochondrial {DNA} ({mtDNA)} was calibrated by setting the date of divergence between primates and ungulates at the Cretaceous-Tertiary boundary (65 million years ago), when the extinction of dinosaurs occurred. A generalized leastsquares method was applied in fitting a model to {mtDNA} sequence data, and the clock gave dates of 92.3$\pm$11.7, 13.3$\pm$1.5, 10.9$\pm$1.2, 3.7$\pm$0.6, and 2.7$\pm$0.6 million years ago (where the second of each pair of numbers is the standard deviation) for the separation of mouse, gibbon, orangutan, gorilla, and chimpanzee, respectively, from the line leading to humans. Although there is some uncertainty in the clock, this dating may pose a problem for the widely believed hypothesis that the bipedal {creatureAustralopithecus} afarensis, which lived some 3.7 million years ago at Laetoli in Tanzania and at Hadar in Ethiopia, was ancestral to man and evolved after the human-ape splitting. Another likelier possibility is that {mtDNA} was transferred through hybridization between a proto-human and a protochimpanzee after the former had developed bipedalism.},
	Author = {Hasegawa, Masami and Kishino, Hirohisa and Yano, Taka-aki},
	Date-Added = {2017-03-21 18:52:48 +0000},
	Date-Modified = {2017-07-30 23:59:50 +0000},
	Journal = {J Mol Evol},
	Number = {2},
	Pages = {160--174},
	Title = {Dating of the human-ape splitting by a molecular clock of mitochondrial {DNA}},
	Volume = {22},
	Year = {1985},
	Bdsk-Url-1 = {http://link.springer.com/article/10.1007/BF02101694},
	Bdsk-Url-2 = {http://dx.doi.org/10.1007/BF02101694}}

@article{yang_1994,
	Abstract = {Two approximate methods are proposed for maximum likelihood phylogenetic estimation, which allow variable rates of substitution across nucleotide sites. Three data sets with quite different characteristics were analyzed to examine empirically the performance of these methods. The first, called the ``discrete gamma model,'' uses several categories of rates to approximate the gamma distribution, with equal probability for each category. The mean of each category is used to represent all the rates falling in the category. The performance of this method is found to be quite good, and four such categories appear to be sufficient to produce both an optimum, or near-optimum fit by the model to the data, and also an acceptable approximation to the continuous distribution. The second method, called ``fixed-rates model,'' classifies sites into several classes according to their rates predicted assuming the star tree. Sites in different classes are then assumed to be evolving at these fixed rates when other tree topologies are evaluated. Analyses of the data sets suggest that this method can produce reasonable results, but it seems to share some properties of a least-squares pairwise comparison; for example, interior branch lengths in nonbest trees are often found to be zero. The computational requirements of the two methods are comparable to that of Felsenstein's (1981, J Mol Evol 17:368--376) model, which assumes a single rate for all the sites.},
	Author = {Yang, Ziheng},
	Date-Added = {2017-03-21 18:52:42 +0000},
	Date-Modified = {2017-07-30 23:11:02 +0000},
	Journal = {J Mol Evol},
	Number = {3},
	Pages = {306--314},
	Title = {Maximum likelihood phylogenetic estimation from {DNA} sequences with variable rates over sites: Approximate methods},
	Volume = {39},
	Year = {1994},
	Bdsk-Url-1 = {http://link.springer.com/article/10.1007/BF00160154},
	Bdsk-Url-2 = {http://dx.doi.org/10.1007/BF00160154}}

@article{bouckaert_beast_2014,
	Abstract = {We present a new open source, extensible and flexible software platform for Bayesian evolutionary analysis called BEAST 2. This software platform is a re-design of the popular BEAST 1 platform to correct structural deficiencies that became evident as the BEAST 1 software evolved. Key among those deficiencies was the lack of post-deployment extensibility. BEAST 2 now has a fully developed package management system that allows third party developers to write additional functionality that can be directly installed to the BEAST 2 analysis platform via a package manager without requiring a new software release of the platform. This package architecture is showcased with a number of recently published new models encompassing birth-death-sampling tree priors, phylodynamics and model averaging for substitution models and site partitioning. A second major improvement is the ability to read/write the entire state of the MCMC chain to/from disk allowing it to be easily shared between multiple instances of the BEAST software. This facilitates checkpointing and better support for multi-processor and high-end computing extensions. Finally, the functionality in new packages can be easily added to the user interface (BEAUti 2) by a simple XML template-based mechanism because BEAST 2 has been re-designed to provide greater integration between the analysis engine and the user interface so that, for example BEAST and BEAUti use exactly the same XML file format.},
	Author = {Bouckaert, Remco and Heled, Joseph and K{\"u}hnert, Denise and Vaughan, Tim and Wu, Chieh-Hsi and Xie, Dong and Suchard, Marc A. and Rambaut, Andrew and Drummond, Alexei J.},
	Date-Added = {2017-03-21 18:52:16 +0000},
	Date-Modified = {2017-07-31 00:14:39 +0000},
	Journal = {PLoS Comput Biol},
	Number = {4},
	Pages = {e1003537},
	Title = {{BEAST} 2: A software platform for {Bayesian} evolutionary analysis},
	Volume = {10},
	Year = {2014},
	Bdsk-Url-1 = {http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003537},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pcbi.1003537}}

@article{dudas_mers-cov_2016,
	Author = {Dudas, Gytis and Rambaut, Andrew},
	Date-Added = {2017-03-17 22:41:24 +0000},
	Date-Modified = {2017-07-31 00:05:51 +0000},
	Journal = {Virus Evol},
	Number = {1},
	Pages = {vev023},
	Title = {{MERS}-{CoV} recombination: implications about the reservoir and potential for adaptation},
	Volume = {2},
	Year = {2016},
	Bdsk-Url-1 = {https://academic.oup.com/ve/article/2/1/vev023/1753363/MERS-CoV-recombination-implications-about-the},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/ve/vev023}}

@article{cotten_2013,
	Abstract = {{SummaryBackground}
Since June, 2012, Middle East respiratory syndrome coronavirus ({MERS}-{CoV}) has, worldwide, caused 104 infections in people including 49 deaths, with 82 cases and 41 deaths reported from Saudi Arabia. In addition to confirming diagnosis, we generated the {MERS}-{CoV} genomic sequences obtained directly from patient samples to provide important information on {MERS}-{CoV} transmission, evolution, and origin.
Methods
Full genome deep sequencing was done on nucleic acid extracted directly from {PCR}-confirmed clinical samples. Viral genomes were obtained from 21 {MERS} cases of which 13 had 100\%, four 85--95\%, and four 30--50\% genome coverage. Phylogenetic analysis of the 21 sequences, combined with nine published {MERS}-{CoV} genomes, was done.
Findings
Three distinct {MERS}-{CoV} genotypes were identified in Riyadh. Phylogeographic analyses suggest the {MERS}-{CoV} zoonotic reservoir is geographically disperse. Selection analysis of the {MERS}-{CoV} genomes reveals the expected accumulation of genetic diversity including changes in the S protein. The genetic diversity in the Al-Hasa cluster suggests that the hospital outbreak might have had more than one virus introduction.
Interpretation
We present the largest number of {MERS}-{CoV} genomes (21) described so far. {MERS}-{CoV} full genome sequences provide greater detail in tracking transmission. Multiple introductions of {MERS}-{CoV} are identified and suggest lower R0 values. Transmission within Saudi Arabia is consistent with either movement of an animal reservoir, animal products, or movement of infected people. Further definition of the exposures responsible for the sporadic introductions of {MERS}-{CoV} into human populations is urgently needed.
Funding
Saudi Arabian Ministry of Health, Wellcome Trust, European Community, and National Institute of Health Research University College London Hospitals Biomedical Research Centre.},
	Author = {Cotten, Matthew and Watson, Simon J and Kellam, Paul and Al-Rabeeah, Abdullah A and Makhdoom, Hatem Q and Assiri, Abdullah and Al-Tawfiq, Jaffar A and Alhakeem, Rafat F and Madani, Hossam and AlRabiah, Fahad A and Hajjar, Sami Al and Al-nassir, Wafa N and Albarrak, Ali and Flemban, Hesham and Balkhy, Hanan H and Alsubaie, Sarah and Palser, Anne L and Gall, Astrid and Bashford-Rogers, Rachael and Rambaut, Andrew and Zumla, Alimuddin I and Memish, Ziad A},
	Date-Added = {2017-03-17 22:33:02 +0000},
	Date-Modified = {2017-07-31 00:07:58 +0000},
	Journal = {Lancet},
	Number = {9909},
	Pages = {1993--2002},
	Title = {Transmission and evolution of the {Middle East} respiratory syndrome coronavirus in {Saudi Arabia}: a descriptive genomic study},
	Volume = {382},
	Year = {2013},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S0140673613618875},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/S0140-6736(13)61887-5}}

@article{fagbo_molecular_2015,
	Abstract = {We investigated an outbreak of Middle East respiratory syndrome (MERS) at King Fahad Medical City (KFMC), Riyadh, Saudi Arabia, during March 29--May 21, 2014. This outbreak involved 45 patients: 8 infected outside KFMC, 13 long-term patients at KFMC, 23 health care workers, and 1 who had an indeterminate source of infection. Sequences of full-length MERS coronavirus (MERS-CoV) from 10 patients and a partial sequence of MERS-CoV from another patient, when compared with other MERS-CoV sequences, demonstrated that this outbreak was part of a larger outbreak that affected multiple health care facilities in Riyadh and possibly arose from a single zoonotic transmission event that occurred in December 2013 (95{\%} highest posterior density interval November 8, 2013--February 10, 2014). This finding suggested continued health care--associated transmission for 5 months. Molecular epidemiology documented multiple external introductions in a seemingly contiguous outbreak and helped support or refute transmission pathways suspected through epidemiologic investigation.},
	Author = {Shamsudeen F. Fagbo and Leila Skakni and Daniel K. W. Chu and Musa A. Garbati and Mercy Joseph and Ahmed M. Hakawi},
	Date-Added = {2017-03-17 22:23:40 +0000},
	Date-Modified = {2017-07-31 00:25:37 +0000},
	Journal = {Emerg Infect Dis},
	Number = {11},
	Pages = {1981},
	Title = {Molecular Epidemiology of Hospital Outbreak of {Middle East} Respiratory Syndrome, {Riyadh}, {Saudi Arabia}, 2014},
	Volume = {21},
	Year = {2015},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/21/11/15-0944},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2111.150944}}

@article{park_acute_2015,
	Abstract = {Camels carry Middle East respiratory syndrome coronavirus, but little is known about infection age or prevalence. We studied {$>$}800 dromedaries of all ages and 15 mother--calf pairs. This syndrome constitutes an acute, epidemic, and time-limited infection in camels {$<$}4 years of age, particularly calves. Delayed social separation of calves might reduce human infection risk.},
	Author = {Sung Sup Park and Ulrich Wernery and Victor M. Corman and Emily Y. M. Wong and Alan K. L. Tsang and Doreen Muth and Susanna K. P. Lau and Kamal Khazanehdari and Florian Zirkel and Mansoor Ali and Peter Nagy and Jutka Juhasz and Renate Wernery and Sunitha Joseph and Ginu Syriac and Shyna K. Elizabeth and Nissy Annie Georgy Patteril and Patrick C. Y. Woo and Christian Drosten},
	Date-Added = {2017-03-17 22:14:09 +0000},
	Date-Modified = {2017-07-31 00:27:08 +0000},
	Journal = {Emerg Infect Dis},
	Number = {6},
	Pages = {1019},
	Title = {Acute {Middle East} Respiratory Syndrome Coronavirus Infection in Livestock Dromedaries, {Dubai}, 2014},
	Volume = {21},
	Year = {2015},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/21/6/15-0038},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2106.150038}}

@article{assiri_hospital_2013,
	Abstract = {A novel coronavirus (MERS-CoV) is causing severe disease in the Middle East. In this report on a hospital outbreak of MERS-CoV infection, 23 confirmed cases and evidence of person-to-person transmission were identified. The median incubation period was 5.2 days.},
	Author = {Assiri, Abdullah and McGeer, Allison and Perl, Trish M. and Price, Connie S. and Al Rabeeah, Abdullah A. and Cummings, Derek A.T. and Alabdullatif, Zaki N. and Assad, Maher and Almulhim, Abdulmohsen and Makhdoom, Hatem and Madani, Hossam and Alhakeem, Rafat and Al-Tawfiq, Jaffar A. and Cotten, Matthew and Watson, Simon J. and Kellam, Paul and Zumla, Alimuddin I. and Memish, Ziad A.},
	Date-Added = {2017-03-17 21:51:48 +0000},
	Date-Modified = {2017-07-31 00:22:06 +0000},
	Journal = {N Engl J Med},
	Number = {5},
	Pages = {407--416},
	Title = {Hospital outbreak of {Middle East} respiratory syndrome coronavirus},
	Volume = {369},
	Year = {2013},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa1306742}}

@article{memish_human_2014,
	Abstract = {We investigated a case of human infection with Middle East respiratory syndrome coronavirus (MERS-CoV) after exposure to infected camels. Analysis of the whole human-derived virus and 15{\%} of the camel-derived virus sequence yielded nucleotide polymorphism signatures suggestive of cross-species transmission. Camels may act as a direct source of human MERS-CoV infection.},
	Author = {Ziad A. Memish and Matthew Cotten and Benjamin Meyer and Simon J. Watson and Abdullah J. Alsahafi and Abdullah A. Al Rabeeah and Victor Max Corman and Andrea Sieberg and Hatem Q. Makhdoom and Abdullah Assiri and Malaki Al Masri and Souhaib Aldabbagh and Berend-Jan Bosch and Martin Beer and Marcel A. M{\"u}ller and Paul Kellam and Christian Drosten},
	Date-Added = {2017-03-17 21:43:22 +0000},
	Date-Modified = {2017-07-31 00:02:57 +0000},
	Journal = {Emerg Infect Dis},
	Number = {6},
	Pages = {1012},
	Title = {Human Infection with {MERS} Coronavirus after Exposure to Infected Camels, {Saudi Arabia}, 2013},
	Volume = {20},
	Year = {2014},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/20/6/14-0402},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2006.140402}}

@article{grubaugh_multiple_2017,
	Abstract = {Zika virus (ZIKV) is causing an unprecedented epidemic linked to severe congenital syndromes1,2. In July 2016, mosquito-borne ZIKV transmission was first reported in the continental United States and since then, hundreds of locally-acquired infections have been reported in Florida3. To gain insights into the timing, source, and likely route(s) of introduction of ZIKV into the continental United States, we tracked the virus from its first detection in Miami, Florida by direct sequencing of ZIKV genomes from infected patients and Aedes aegypti mosquitoes. We show that at least four distinct ZIKV introductions contributed to the outbreak in Florida and that local transmission likely started in the spring of 2016 - several months before its initial detection. By analyzing surveillance and genetic data, we discovered that ZIKV moved among transmission zones in Miami. Our analyses show that most introductions are phylogenetically linked to the Caribbean, a finding corroborated by the high incidence rates and traffic volumes from the region into the Miami area. By comparing mosquito abundance and travel flows, we describe the areas of southern Florida that are especially vulnerable to ZIKV introductions. Our study provides a deeper understanding of how ZIKV initiates and sustains transmission in new regions.},
	Author = {Grubaugh, Nathan D. and Ladner, Jason T. and Kraemer, Moritz UG and Dudas, Gytis and Tan, Amanda L. and Gangavarapu, Karthik and Wiley, Michael R. and White, Stephen and Th{\'e}z{\'e}, Julien and Magnani, Diogo M. and Prieto, Karla and Reyes, Daniel and Bingham, Andrea and Paul, Lauren M. and Robles-Sikisaka, Refugio and Oliveira, Glenn and Pronty, Darryl and Metsky, Hayden C. and Baniecki, Mary Lynn and Barnes, Kayla G. and Chak, Bridget and Freije, Catherine A. and Gladden-Young, Adrianne and Gnirke, Andreas and Luo, Cynthia and MacInnis, Bronwyn and Matranga, Christian B. and Park, Daniel J. and Qu, James and Schaffner, Stephen F. and Tomkins-Tinch, Christopher and West, Kendra L. and Winnicki, Sarah M. and Wohl, Shirlee and Yozwiak, Nathan L. and Quick, Joshua and Fauver, Joseph R. and Khan, Kamran and Brent, Shannon E. and Reiner, Robert C. and Lichtenberger, Paola N. and Ricciardi, Michael and Bailey, Varian K. and Watkins, David I. and Cone, Marshall R. and Kopp, Edgar W. and Hogan, Kelly N. and Cannons, Andrew C. and Jean, Reynald and Garry, Robert F. and Loman, Nicholas J. and Faria, Nuno R. and Porcelli, Mario C. and Vasquez, Chalmers and Nagle, Elyse R. and Cummings, Derek AT and Stanek, Danielle and Rambaut, Andrew and Sanchez-Lockhart, Mariano and Sabeti, Pardis C. and Gillis, Leah D. and Michael, Scott F. and Bedford, Trevor and Pybus, Oliver G. and Isern, Sharon and Palacios, Gustavo and Andersen, Kristian G.},
	Date-Added = {2017-03-17 21:40:18 +0000},
	Date-Modified = {2017-07-30 22:22:36 +0000},
	Journal = {Nature},
	Pages = {401--405},
	Title = {Genomic epidemiology reveals multiple introductions of {Zika} virus into the {United States}},
	Volume = {546},
	Year = {2017},
	Bdsk-Url-1 = {http://biorxiv.org/content/early/2017/02/03/104794},
	Bdsk-Url-2 = {http://dx.doi.org/10.1101/104794}}

@article{gire_genomic_2014,
	Abstract = {Evolution of Ebola virus over time
The high rate of mortality in the current Ebola epidemic has made it difficult for researchers to collect samples of the virus and study its evolution. Gire et al. describe Ebola epidemiology on the basis of 99 whole-genome sequences, including samples from 78 affected individuals. The authors analyzed changes in the viral sequence and conclude that the current outbreak probably resulted from the spread of the virus from central Africa in the past decade. The outbreak started from a single transmission event from an unknown animal reservoir into the human population. Two viral lineages from Guinea then spread from person to person into Sierra Leone.
Science, this issue p. 1369
In its largest outbreak, Ebola virus disease is spreading through Guinea, Liberia, Sierra Leone, and Nigeria. We sequenced 99 Ebola virus genomes from 78 patients in Sierra Leone to {\textasciitilde}2000× coverage. We observed a rapid accumulation of interhost and intrahost genetic variation, allowing us to characterize patterns of viral transmission over the initial weeks of the epidemic. This West African variant likely diverged from central African lineages around 2004, crossed from Guinea to Sierra Leone in May 2014, and has exhibited sustained human-to-human transmission subsequently, with no evidence of additional zoonotic sources. Because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.
Sequencing the genome of Ebola virus disease provides tracking information.
Sequencing the genome of Ebola virus disease provides tracking information.},
	Author = {Gire, Stephen K. and Goba, Augustine and Andersen, Kristian G. and Sealfon, Rachel S. G. and Park, Daniel J. and Kanneh, Lansana and Jalloh, Simbirie and Momoh, Mambu and Fullah, Mohamed and Dudas, Gytis and Wohl, Shirlee and Moses, Lina M. and Yozwiak, Nathan L. and Winnicki, Sarah and Matranga, Christian B. and Malboeuf, Christine M. and Qu, James and Gladden, Adrianne D. and Schaffner, Stephen F. and Yang, Xiao and Jiang, Pan-Pan and Nekoui, Mahan and Colubri, Andres and Coomber, Moinya Ruth and Fonnie, Mbalu and Moigboi, Alex and Gbakie, Michael and Kamara, Fatima K. and Tucker, Veronica and Konuwa, Edwin and Saffa, Sidiki and Sellu, Josephine and Jalloh, Abdul Azziz and Kovoma, Alice and Koninga, James and Mustapha, Ibrahim and Kargbo, Kandeh and Foday, Momoh and Yillah, Mohamed and Kanneh, Franklyn and Robert, Willie and Massally, James L. B. and Chapman, Sin{\'e}ad B. and Bochicchio, James and Murphy, Cheryl and Nusbaum, Chad and Young, Sarah and Birren, Bruce W. and Grant, Donald S. and Scheiffelin, John S. and Lander, Eric S. and Happi, Christian and Gevao, Sahr M. and Gnirke, Andreas and Rambaut, Andrew and Garry, Robert F. and Khan, S. Humarr and Sabeti, Pardis C.},
	Copyright = {Copyright {\copyright} 2014, American Association for the Advancement of Science},
	Date-Added = {2017-03-17 21:40:14 +0000},
	Date-Modified = {2017-03-17 21:40:14 +0000},
	Doi = {10.1126/science.1259657},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/NEXWTMU7/Gire et al. - 2014 - Genomic surveillance elucidates Ebola virus origin.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/T7U3K46I/1369.html:text/html},
	Issn = {0036-8075, 1095-9203},
	Journal = {Science},
	Language = {en},
	Month = sep,
	Number = {6202},
	Pages = {1369--1372},
	Pmid = {25214632},
	Title = {Genomic surveillance elucidates {Ebola} virus origin and transmission during the 2014 outbreak},
	Url = {http://science.sciencemag.org/content/345/6202/1369},
	Urldate = {2017-03-17},
	Volume = {345},
	Year = {2014},
	Bdsk-Url-1 = {http://science.sciencemag.org/content/345/6202/1369},
	Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1259657}}

@article{arias_rapid_2016,
	Author = {Arias, Armando and Watson, Simon J. and Asogun, Danny and Tobin, Ekaete Alice and Lu, Jia and Phan, My V. T. and Jah, Umaru and Wadoum, Raoul Emeric Guetiya and Meredith, Luke and Thorne, Lucy and Caddy, Sarah and Tarawalie, Alimamy and Langat, Pinky and Dudas, Gytis and Faria, Nuno R. and Dellicour, Simon and Kamara, Abdul and Kargbo, Brima and Kamara, Brima Osaio and Gevao, Sahr and Cooper, Daniel and Newport, Matthew and Horby, Peter and Dunning, Jake and Sahr, Foday and Brooks, Tim and Simpson, Andrew J. H. and Groppelli, Elisabetta and Liu, Guoying and Mulakken, Nisha and Rhodes, Kate and Akpablie, James and Yoti, Zabulon and Lamunu, Margaret and Vitto, Esther and Otim, Patrick and Owilli, Collins and Boateng, Isaac and Okoror, Lawrence and Omomoh, Emmanuel and Oyakhilome, Jennifer and Omiunu, Racheal and Yemisis, Ighodalo and Adomeh, Donatus and Ehikhiametalor, Solomon and Akhilomen, Patience and Aire, Chris and Kurth, Andreas and Cook, Nicola and Baumann, Jan and Gabriel, Martin and W{\"o}lfel, Roman and Di Caro, Antonino and Carroll, Miles W. and G{\"u}nther, Stephan and Redd, John and Naidoo, Dhamari and Pybus, Oliver G. and Rambaut, Andrew and Kellam, Paul and Goodfellow, Ian and Cotten, Matthew},
	Date-Added = {2017-03-17 21:37:33 +0000},
	Date-Modified = {2017-03-17 21:37:33 +0000},
	Doi = {10.1093/ve/vew016},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/QWKDRE3K/Arias et al. - 2016 - Rapid outbreak sequencing of Ebola virus in Sierra.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/3NWWCPNC/Rapid-outbreak-sequencing-of-Ebola-virus-in-Sierra.html:text/html},
	Journal = {Virus Evolution},
	Month = jan,
	Number = {1},
	Title = {Rapid outbreak sequencing of {Ebola} virus in {Sierra} {Leone} identifies transmission chains linked to sporadic cases},
	Url = {https://academic.oup.com/ve/article/2/1/vew016/1753554/Rapid-outbreak-sequencing-of-Ebola-virus-in-Sierra},
	Urldate = {2017-03-17},
	Volume = {2},
	Year = {2016},
	Bdsk-Url-1 = {https://academic.oup.com/ve/article/2/1/vew016/1753554/Rapid-outbreak-sequencing-of-Ebola-virus-in-Sierra},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/ve/vew016}}

@article{reusken_2014,
	Author = {Reusken, Chantal B.E.M. and Messadi, Lilia and Feyisa, Ashenafi and Ularamu, Hussaini and Godeke, Gert-Jan and Danmarwa, Agom and Dawo, Fufa and Jemli, Mohamed and Melaku, Simenew and Shamaki, David and Woma, Yusuf and Wungak, Yiltawe and Gebremedhin, Endrias Zewdu and Zutt, Ilse and Bosch, Berend-Jan and Haagmans, Bart L. and Koopmans, Marion P.G.},
	Date-Added = {2017-03-17 21:31:09 +0000},
	Date-Modified = {2017-07-31 00:02:13 +0000},
	Journal = {Emerg Infect Dis},
	Number = {8},
	Pages = {1370--1374},
	Title = {Geographic distribution of {MERS} coronavirus among dromedary camels, {Africa}},
	Volume = {20},
	Year = {2014},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/20/8/14-0590_article},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2008.140590}}

@article{chu_2014,
	Author = {Chu, Daniel K.W. and Poon, Leo L.M. and Gomaa, Mokhtar M. and Shehata, Mahmoud M. and Perera, Ranawaka A.P.M. and Abu Zeid, Dina and El Rifay, Amira S. and Siu, Lewis Y. and Guan, Yi and Webby, Richard J. and Ali, Mohamed A. and Peiris, Malik and Kayali, Ghazi},
	Date-Added = {2017-03-17 21:30:42 +0000},
	Date-Modified = {2017-07-31 00:09:56 +0000},
	Journal = {Emerg Infect Dis},
	Number = {6},
	Pages = {1049--1053},
	Title = {{MERS} Coronaviruses in Dromedary Camels, {Egypt}},
	Volume = {20},
	Year = {2014},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/20/6/14-0299_article},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2006.140299}}

@article{corman_antibodies_2014,
	Author = {Corman, Victor M. and Jores, Joerg and Meyer, Benjamin and Younan, Mario and Liljander, Anne and Said, Mohammed Y. and Gluecks, Ilona and Lattwein, Erik and Bosch, Berend-Jan and Drexler, Jan Felix and Bornstein, Set and Drosten, Christian and M{\"u}ller, Marcel A.},
	Date-Added = {2017-03-17 21:28:52 +0000},
	Date-Modified = {2017-07-31 00:09:12 +0000},
	Journal = {Emerg Infect Dis},
	Number = {8},
	Pages = {1319--1322},
	Title = {Antibodies against {MERS} Coronavirus in Dromedary Camels, {Kenya}, 1992--2013},
	Volume = {20},
	Year = {2014},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/20/8/14-0596_article},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2008.140596}}

@article{muller_2014,
	Author = {M{\"u}ller, Marcel A. and Corman, Victor Max and Jores, Joerg and Meyer, Benjamin and Younan, Mario and Liljander, Anne and Bosch, Berend-Jan and Lattwein, Erik and Hilali, Mosaad and Musa, Bakri E. and Bornstein, Set and Drosten, Christian},
	Date-Added = {2017-03-17 21:27:31 +0000},
	Date-Modified = {2017-07-31 00:02:50 +0000},
	Journal = {Emerg Infect Dis},
	Number = {12},
	Title = {{MERS} Coronavirus Neutralizing Antibodies in Camels, {Eastern Africa}, 1983--1997},
	Volume = {20},
	Year = {2014},
	Bdsk-Url-1 = {http://wwwnc.cdc.gov/eid/article/20/12/14-1026_article},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2012.141026}}

@article{muller_presence_2015,
	Abstract = {SummaryBackground
Scientific evidence suggests that dromedary camels are the intermediary host for the Middle East respiratory syndrome coronavirus (MERS-CoV). However, the actual number of infections in people who have had contact with camels is unknown and most index patients cannot recall any such contact. We aimed to do a nationwide serosurvey in Saudi Arabia to establish the prevalence of MERS-CoV antibodies, both in the general population and in populations of individuals who have maximum exposure to camels.
Methods
In the cross-sectional serosurvey, we tested human serum samples obtained from healthy individuals older than 15 years who attended primary health-care centres or participated in a national burden-of-disease study in all 13 provinces of Saudi Arabia. Additionally, we tested serum samples from shepherds and abattoir workers with occupational exposure to camels. Samples were screened by recombinant ELISA and MERS-CoV seropositivity was confirmed by recombinant immunofluorescence and plaque reduction neutralisation tests. We used two-tailed Mann Whitney U exact tests, χ2, and Fisher's exact tests to analyse the data.
Findings
Between Dec 1, 2012, and Dec 1, 2013, we obtained individual serum samples from 10 009 individuals. Anti-MERS-CoV antibodies were confirmed in 15 (0·15\%; 95\% CI 0·09--0·24) of 10 009 people in six of the 13 provinces. The mean age of seropositive individuals was significantly younger than that of patients with reported, laboratory-confirmed, primary Middle Eastern respiratory syndrome (43·5 years [SD 17·3] vs 53·8 years [17·5]; p=0·008). Men had a higher antibody prevalence than did women (11 [0·25\%] of 4341 vs two [0·05\%] of 4378; p=0·028) and antibody prevalence was significantly higher in central versus coastal provinces (14 [0·26\%] of 5479 vs one [0·02\%] of 4529; p=0·003). Compared with the general population, seroprevalence of MERS-CoV antibodies was significantly increased by 15 times in shepherds (two [2·3\%] of 87, p=0·0004) and by 23 times in slaughterhouse workers (five [3·6\%] of 140; p\&lt;0·0001).
Interpretation
Seroprevalence of MERS-CoV antibodies was significantly higher in camel-exposed individuals than in the general population. By simple multiplication, a projected 44 951 (95\% CI 26 971--71 922) individuals older than 15 years might be seropositive for MERS-CoV in Saudi Arabia. These individuals might be the source of infection for patients with confirmed MERS who had no previous exposure to camels.
Funding
European Union, German Centre for Infection Research, Federal Ministry of Education and Research, German Research Council, and Ministry of Health of Saudi Arabia.},
	Author = {M{\"u}ller, Marcel A and Meyer, Benjamin and Corman, Victor M and Al-Masri, Malak and Turkestani, Abdulhafeez and Ritz, Daniel and Sieberg, Andrea and Aldabbagh, Souhaib and Bosch, Berend-J and Lattwein, Erik and Alhakeem, Raafat F and Assiri, Abdullah M and Albarrak, Ali M and Al-Shangiti, Ali M and Al-Tawfiq, Jaffar A and Wikramaratna, Paul and Alrabeeah, Abdullah A and Drosten, Christian and Memish, Ziad A},
	Date-Added = {2017-03-17 21:14:54 +0000},
	Date-Modified = {2017-07-30 23:51:45 +0000},
	Journal = {Lancet Infect Dis},
	Number = {5},
	Pages = {559--564},
	Title = {Presence of {Middle} {East} respiratory syndrome coronavirus antibodies in {Saudi} {Arabia}: a nationwide, cross-sectional, serological study},
	Volume = {15},
	Year = {2015},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S1473309915700903},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/S1473-3099(15)70090-3}}

@article{cauchemez_2014,
	Abstract = {{SummaryBackground}
The novel Middle East respiratory syndrome coronavirus ({MERS}-{CoV}) had, as of Aug 8, 2013, caused 111 virologically confirmed or probable human cases of infection worldwide. We analysed epidemiological and genetic data to assess the extent of human infection, the performance of case detection, and the transmission potential of {MERS}-{CoV} with and without control measures.
Methods
We assembled a comprehensive database of all confirmed and probable cases from public sources and estimated the incubation period and generation time from case cluster data. Using data of numbers of visitors to the Middle East and their duration of stay, we estimated the number of symptomatic cases in the Middle East. We did independent analyses, looking at the growth in incident clusters, the growth in viral population, the reproduction number of cluster index cases, and cluster sizes to characterise the dynamical properties of the epidemic and the transmission scenario.
Findings
The estimated number of symptomatic cases up to Aug 8, 2013, is 940 (95\% {CI} 290--2200), indicating that at least 62\% of human symptomatic cases have not been detected. We find that the case-fatality ratio of primary cases detected via routine surveillance (74\%; 95\% {CI} 49--91) is biased upwards because of detection bias; the case-fatality ratio of secondary cases was 20\% (7--42). Detection of milder cases (or clinical management) seemed to have improved in recent months. Analysis of human clusters indicated that chains of transmission were not self-sustaining when infection control was implemented, but that R in the absence of controls was in the range 0·8--1·3. Three independent data sources provide evidence that R cannot be much above 1, with an upper bound of 1·2--1·5.
Interpretation
By showing that a slowly growing epidemic is underway either in human beings or in an animal reservoir, quantification of uncertainty in transmissibility estimates, and provision of the first estimates of the scale of the epidemic and extent of case detection biases, we provide valuable information for more informed risk assessment.
Funding
Medical Research Council, Bill \&amp; Melinda Gates Foundation, {EU} {FP}7, and National Institute of General Medical Sciences.},
	Author = {Cauchemez, Simon and Fraser, Christophe and Van Kerkhove, Maria D and Donnelly, Christl A and Riley, Steven and Rambaut, Andrew and Enouf, Vincent and van der Werf, Sylvie and Ferguson, Neil M},
	Date-Added = {2017-03-17 20:39:48 +0000},
	Date-Modified = {2017-03-17 20:39:48 +0000},
	Doi = {10.1016/S1473-3099(13)70304-9},
	File = {ScienceDirect Full Text PDF:/Users/admin/Library/Application Support/Firefox/Profiles/tit72ymn.default/zotero/storage/T4PUZBEN/Cauchemez et al. - 2014 - Middle East respiratory syndrome coronavirus quan.pdf:application/pdf;ScienceDirect Snapshot:/Users/admin/Library/Application Support/Firefox/Profiles/tit72ymn.default/zotero/storage/3VXPW39M/S1473309913703049.html:text/html},
	Issn = {1473-3099},
	Journal = {The Lancet Infectious Diseases},
	Month = jan,
	Number = {1},
	Pages = {50--56},
	Shorttitle = {Middle East respiratory syndrome coronavirus},
	Title = {Middle East respiratory syndrome coronavirus: quantification of the extent of the epidemic, surveillance biases, and transmissibility},
	Url = {http://www.sciencedirect.com/science/article/pii/S1473309913703049},
	Urldate = {2014-12-18},
	Volume = {14},
	Year = {2014},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S1473309913703049},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/S1473-3099(13)70304-9}}

@article{reusken_2013,
	Abstract = {{SummaryBackground}
A new betacoronavirus---Middle East respiratory syndrome coronavirus ({MERS}-{CoV})---has been identified in patients with severe acute respiratory infection. Although related viruses infect bats, molecular clock analyses have been unable to identify direct ancestors of {MERS}-{CoV}. Anecdotal exposure histories suggest that patients had been in contact with dromedary camels or goats. We investigated possible animal reservoirs of {MERS}-{CoV} by assessing specific serum antibodies in livestock.
Methods
We took sera from animals in the Middle East (Oman) and from elsewhere (Spain, Netherlands, Chile). Cattle (n=80), sheep (n=40), goats (n=40), dromedary camels (n=155), and various other camelid species (n=34) were tested for specific serum {IgG} by protein microarray using the receptor-binding S1 subunits of spike proteins of {MERS}-{CoV}, severe acute respiratory syndrome coronavirus, and human coronavirus {OC}43. Results were confirmed by virus neutralisation tests for {MERS}-{CoV} and bovine coronavirus.
Findings
50 of 50 (100\%) sera from Omani camels and 15 of 105 (14\%) from Spanish camels had protein-specific antibodies against {MERS}-{CoV} spike. Sera from European sheep, goats, cattle, and other camelids had no such antibodies. {MERS}-{CoV} neutralising antibody titres varied between 1/320 and 1/2560 for the Omani camel sera and between 1/20 and 1/320 for the Spanish camel sera. There was no evidence for cross-neutralisation by bovine coronavirus antibodies.
Interpretation
{MERS}-{CoV} or a related virus has infected camel populations. Both titres and seroprevalences in sera from different locations in Oman suggest widespread infection.
Funding
European Union, European Centre For Disease Prevention and Control, Deutsche Forschungsgemeinschaft.},
	Author = {Reusken, Chantal BEM and Haagmans, Bart L and M\"{u}ller, Marcel A and Gutierrez, Carlos and Godeke, Gert-Jan and Meyer, Benjamin and Muth, Doreen and Raj, V Stalin and Vries, Laura Smits-De and Corman, Victor M and Drexler, Jan-Felix and Smits, Saskia L and El Tahir, Yasmin E and De Sousa, Rita and van Beek, Janko and Nowotny, Norbert and van Maanen, Kees and Hidalgo-Hermoso, Ezequiel and Bosch, Berend-Jan and Rottier, Peter and Osterhaus, Albert and Gort\'{a}zar-Schmidt, Christian and Drosten, Christian and Koopmans, Marion PG},
	Date-Added = {2017-03-17 20:30:57 +0000},
	Date-Modified = {2017-11-15 18:19:13 +0000},
	Journal = {Lancet Infect Dis},
	Number = {10},
	Pages = {859--866},
	Title = {{Middle East} respiratory syndrome coronavirus neutralising serum antibodies in dromedary camels: a comparative serological study},
	Volume = {13},
	Year = {2013},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S1473309913701646},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/S1473-3099(13)70164-6}}

@article{reusken_occupational_2015,
	Abstract = {PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.},
	Author = {Reusken, Chantal B. E. M. and Farag, Elmoubasher A. B. A. and Haagmans, Bart L. and Mohran, Khaled A. and Godeke, Gert-Jan and V and Raj, Stalin and Alhajri, Farhoud and Al-Marri, Salih A. and Al-Romaihi, Hamad E. and Al-Thani, Mohamed and Bosch, Berend-Jan and Eijk, Annemiek A. van der and El-Sayed, Ahmed M. and Ibrahim, Adel K. and Al-Molawi, N. and M{\"u}ller, Marcel A. and Pasha, Syed K. and Drosten, Christian and AlHajri, Mohd M. and Koopmans, Marion P. G.},
	Date-Added = {2017-03-17 20:28:56 +0000},
	Date-Modified = {2017-07-31 00:02:17 +0000},
	Journal = {Emerg Infect Dis},
	Number = {8},
	Pages = {1422},
	Title = {Occupational exposure to dromedaries and risk for {MERS}-{CoV} infection, {Qatar}, 2013--2014},
	Volume = {21},
	Year = {2015},
	Bdsk-Url-1 = {/pmcc/articles/PMC4517733/?report=abstract},
	Bdsk-Url-2 = {http://dx.doi.org/10.3201/eid2108.150481}}

@article{group_state_2013,
	Author = {{The WHO MERS-CoV Research Group}},
	Date-Added = {2017-03-17 00:06:15 +0000},
	Date-Modified = {2017-07-31 00:31:21 +0000},
	Journal = {PLoS Curr},
	Title = {State of knowledge and data gaps of {Middle East} respiratory syndrome coronavirus ({MERS-CoV}) in humans},
	Volume = {Edition 1},
	Year = {2013},
	Bdsk-Url-1 = {http://currents.plos.org/outbreaks/article/state-of-knowledge-and-data-gaps-of-middle-east-respiratory-syndrome-coronavirus-mers-cov-in-humans-2/},
	Bdsk-Url-2 = {http://dx.doi.org/10.1371/currents.outbreaks.0bf719e352e7478f8ad85fa30127ddb8}}

@article{assiri_2013,
	Abstract = {{SummaryBackground}
Middle East respiratory syndrome ({MERS}) is a new human disease caused by a novel coronavirus ({CoV}). Clinical data on {MERS}-{CoV} infections are scarce. We report epidemiological, demographic, clinical, and laboratory characteristics of 47 cases of {MERS}-{CoV} infections, identify knowledge gaps, and define research priorities.
Methods
We abstracted and analysed epidemiological, demographic, clinical, and laboratory data from confirmed cases of sporadic, household, community, and health-care-associated {MERS}-{CoV} infections reported from Saudi Arabia between Sept 1, 2012, and June 15, 2013. Cases were confirmed as having {MERS}-{CoV} by real-time {RT}-{PCR}.
Findings
47 individuals (46 adults, one child) with laboratory-confirmed {MERS}-{CoV} disease were identified; 36 (77\%) were male (male:female ratio 3·3:1). 28 patients died, a 60\% case-fatality rate. The case-fatality rate rose with increasing age. Only two of the 47 cases were previously healthy; most patients (45 [96\%]) had underlying comorbid medical disorders, including diabetes (32 [68\%]), hypertension (16 [34\%]), chronic cardiac disease (13 [28\%]), and chronic renal disease (23 [49\%]). Common symptoms at presentation were fever (46 [98\%]), fever with chills or rigors (41 [87\%]), cough (39 [83\%]), shortness of breath (34 [72\%]), and myalgia (15 [32\%]). Gastrointestinal symptoms were also frequent, including diarrhoea (12 [26\%]), vomiting (ten [21\%]), and abdominal pain (eight [17\%]). All patients had abnormal findings on chest radiography, ranging from subtle to extensive unilateral and bilateral abnormalities. Laboratory analyses showed raised concentrations of lactate dehydrogenase (23 [49\%]) and aspartate aminotransferase (seven [15\%]) and thrombocytopenia (17 [36\%]) and lymphopenia (16 [34\%]).
Interpretation
Disease caused by {MERS}-{CoV} presents with a wide range of clinical manifestations and is associated with substantial mortality in admitted patients who have medical comorbidities. Major gaps in our knowledge of the epidemiology, community prevalence, and clinical spectrum of infection and disease need urgent definition.
Funding
None.},
	Author = {Assiri, Abdullah and Al-Tawfiq, Jaffar A and Al-Rabeeah, Abdullah A and Al-Rabiah, Fahad A and Al-Hajjar, Sami and Al-Barrak, Ali and Flemban, Hesham and Al-Nassir, Wafa N and Balkhy, Hanan H and Al-Hakeem, Rafat F and Makhdoom, Hatem Q and Zumla, Alimuddin I and Memish, Ziad A},
	Date-Added = {2017-03-16 23:58:23 +0000},
	Date-Modified = {2017-07-31 00:23:30 +0000},
	Journal = {Lancet Infect Dis},
	Number = {9},
	Pages = {752--761},
	Title = {Epidemiological, demographic, and clinical characteristics of 47 cases of {Middle East} respiratory syndrome coronavirus disease from {Saudi Arabia}: a descriptive study},
	Volume = {13},
	Year = {2013},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S1473309913702044},
	Bdsk-Url-2 = {http://dx.doi.org/10.1016/S1473-3099(13)70204-4}}

@article{zaki_isolation_2012,
	Abstract = {On June 24, 2012, a 60-year-old man died of progressive respiratory infection in Saudi Arabia. A novel coronavirus was identified as a potential cause of this severe illness. Subsequently, a second patient was reported to have severe illness associated with this coronavirus.},
	Author = {Zaki, Ali M. and van Boheemen, Sander and Bestebroer, Theo M. and Osterhaus, Albert D.M.E. and Fouchier, Ron A.M.},
	Date-Added = {2017-03-16 23:40:24 +0000},
	Date-Modified = {2017-07-30 23:09:29 +0000},
	Journal = {N Engl J Med},
	Number = {19},
	Pages = {1814--1820},
	Title = {Isolation of a novel coronavirus from a man with pneumonia in {Saudi Arabia}},
	Volume = {367},
	Year = {2012},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa1211721}}

@article{boheemen_genomic_2012,
	Abstract = {A novel human coronavirus (HCoV-EMC/2012) was isolated from a man with acute pneumonia and renal failure in June 2012. This report describes the complete genome sequence, genome organization, and expression strategy of HCoV-EMC/2012 and its relation with known coronaviruses. The genome contains 30,119 nucleotides and contains at least 10 predicted open reading frames, 9 of which are predicted to be expressed from a nested set of seven subgenomic mRNAs. Phylogenetic analysis of the replicase gene of coronaviruses with completely sequenced genomes showed that HCoV-EMC/2012 is most closely related to Tylonycteris bat coronavirus HKU4 (BtCoV-HKU4) and Pipistrellus bat coronavirus HKU5 (BtCoV-HKU5), which prototype two species in lineage C of the genus Betacoronavirus. In accordance with the guidelines of the International Committee on Taxonomy of Viruses, and in view of the 75\% and 77\% amino acid sequence identity in 7 conserved replicase domains with BtCoV-HKU4 and BtCoV-HKU5, respectively, we propose that HCoV-EMC/2012 prototypes a novel species in the genus Betacoronavirus. HCoV-EMC/2012 may be most closely related to a coronavirus detected in Pipistrellus pipistrellus in The Netherlands, but because only a short sequence from the most conserved part of the RNA-dependent RNA polymerase-encoding region of the genome was reported for this bat virus, its genetic distance from HCoV-EMC remains uncertain. HCoV-EMC/2012 is the sixth coronavirus known to infect humans and the first human virus within betacoronavirus lineage C.
IMPORTANCE Coronaviruses are capable of infecting humans and many animal species. Most infections caused by human coronaviruses are relatively mild. However, the outbreak of severe acute respiratory syndrome (SARS) caused by SARS-CoV in 2002 to 2003 and the fatal infection of a human by HCoV-EMC/2012 in 2012 show that coronaviruses are able to cause severe, sometimes fatal disease in humans. We have determined the complete genome of HCoV-EMC/2012 using an unbiased virus discovery approach involving next-generation sequencing techniques, which enabled subsequent state-of-the-art bioinformatics, phylogenetics, and taxonomic analyses. By establishing its complete genome sequence, HCoV-EMC/2012 was characterized as a new genotype which is closely related to bat coronaviruses that are distant from SARS-CoV. We expect that this information will be vital to rapid advancement of both clinical and vital research on this emerging pathogen.},
	Author = {Boheemen, Sander van and Graaf, Miranda de and Lauber, Chris and Bestebroer, Theo M. and Raj, V. Stalin and Zaki, Ali Moh and Osterhaus, Albert D. M. E. and Haagmans, Bart L. and Gorbalenya, Alexander E. and Snijder, Eric J. and Fouchier, Ron A. M.},
	Date-Added = {2017-03-16 23:40:19 +0000},
	Date-Modified = {2017-07-31 00:17:37 +0000},
	Journal = {mBio},
	Number = {6},
	Pages = {e00473--12},
	Title = {Genomic characterization of a newly discovered coronavirus associated with acute respiratory distress syndrome in humans},
	Volume = {3},
	Year = {2012},
	Bdsk-Url-1 = {http://mbio.asm.org/content/3/6/e00473-12},
	Bdsk-Url-2 = {http://dx.doi.org/10.1128/mBio.00473-12}}

@article{azhar_evidence_2014,
	Abstract = {The source of Middle East respiratory syndrome coronavirus infection in humans is unclear, although bats and camels are suspected animal reservoirs. In this report, direct transmission of a fatal human case is tightly linked to a camel by epidemiologic, serologic, and virologic data.},
	Author = {Azhar, Esam I. and El-Kafrawy, Sherif A. and Farraj, Suha A. and Hassan, Ahmed M. and Al-Saeed, Muneera S. and Hashem, Anwar M. and Madani, Tariq A.},
	Doi = {10.1056/NEJMoa1401505},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/FPARJ8DR/Azhar et al. - 2014 - Evidence for Camel-to-Human Transmission of MERS C.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/2BSI4VXV/NEJMoa1401505.html:text/html},
	Issn = {0028-4793},
	Journal = {New England Journal of Medicine},
	Month = jun,
	Number = {26},
	Pages = {2499--2505},
	Pmid = {24896817},
	Title = {Evidence for {Camel}-to-{Human} {Transmission} of {MERS} {Coronavirus}},
	Url = {http://dx.doi.org/10.1056/NEJMoa1401505},
	Urldate = {2017-02-28},
	Volume = {370},
	Year = {2014},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa1401505}}

@article{vaughan_efficient_2014,
	Author = {Vaughan, Timothy G. and K{\"u}hnert, Denise and Popinga, Alex and Welch, David and Drummond, Alexei J.},
	Doi = {10.1093/bioinformatics/btu201},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/AVIWI2IR/Vaughan et al. - 2014 - Efficient Bayesian inference under the structured .pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/JBEMBNVU/btu201.html:text/html},
	Issn = {1367-4803},
	Journal = {Bioinformatics},
	Month = aug,
	Number = {16},
	Pages = {2272--2279},
	Title = {Efficient {Bayesian} inference under the structured coalescent},
	Url = {https://academic.oup.com/bioinformatics/article/30/16/2272/2748160/Efficient-Bayesian-inference-under-the-structured},
	Urldate = {2017-03-01},
	Volume = {30},
	Year = {2014},
	Bdsk-Url-1 = {https://academic.oup.com/bioinformatics/article/30/16/2272/2748160/Efficient-Bayesian-inference-under-the-structured},
	Bdsk-Url-2 = {http://dx.doi.org/10.1093/bioinformatics/btu201}}

@unpublished{who_mers_guidelines_2016,
	Abstract = {Between 6 and 13 December 2016 the National IHR Focal Point of Saudi Arabia reported ten (10) additional cases of Middle East Respiratory Syndrome (MERS) including two (2) fatal cases. Three (3) deaths among previously reported MERS cases were also reported.},
	Author = {{World Health Organization}},
	Date-Modified = {2017-08-07 00:06:48 +0000},
	Note = {Available at \url{http://www.who.int/csr/don/19-december-2016-2-mers-saudi-arabia/en/}},
	Title = {Disease outbreak news -- 2016 December 19},
	Year = {2016},
	Bdsk-Url-1 = {http://www.who.int/csr/don/19-december-2016-2-mers-saudi-arabia/en/}}

@article{lanciault_pausing_2006,
	Abstract = {Retroviruses package two copies of genomic RNA into viral particles. During the minus-sense DNA synthesis step of reverse transcription, the nascent DNA can transfer multiple times between the two copies of the genome, resulting in recombination. The mechanism for this process is similar to the process of obligate strand transfers mediated by the repeat and primer binding site sequences. The location at which the DNA 3′ terminus completely transfers to the second RNA strand defines the point of crossover. Previous work in vitro demonstrated that reverse transcriptase pausing has a significant impact on the location of the crossover, with a proportion of complete transfer events occurring very close to pause sites. The role of pausing in vivo, however, is not clearly understood. By employing a murine leukemia virus-based single-cycle infection assay, strong pausing was shown to increase the probability of recombination, as reflected in the reconstitution of green fluorescent protein expression. The infection assay results were directly correlated with the presence of strong pause sites in reverse transcriptase primer extension assays in vitro. Conversely, when pausing was diminished in vitro, without changing the sequence of the RNA template involved in recombination, there was a significant reduction in recombination in vivo. Together, these data demonstrate that reverse transcriptase pausing, as observed in vitro, directly correlates with recombination during minus-sense DNA synthesis in vivo.},
	Author = {Lanciault, Christian and Champoux, James J.},
	Doi = {10.1128/JVI.80.5.2483-2494.2006},
	File = {Full Text PDF:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/FRGDAUB3/Lanciault and Champoux - 2006 - Pausing during Reverse Transcription Increases the.pdf:application/pdf;Snapshot:/Users/evogytis/Library/Application Support/Zotero/Profiles/1sfxzhn6.default/zotero/storage/MRC7CFDR/2483.html:text/html},
	Issn = {0022-538X, 1098-5514},
	Journal = {Journal of Virology},
	Language = {en},
	Month = mar,
	Number = {5},
	Pages = {2483--2494},
	Pmid = {16474155},
	Title = {Pausing during {Reverse} {Transcription} {Increases} the {Rate} of {Retroviral} {Recombination}},
	Url = {http://jvi.asm.org/content/80/5/2483},
	Urldate = {2017-03-03},
	Volume = {80},
	Year = {2006},
	Bdsk-Url-1 = {http://jvi.asm.org/content/80/5/2483},
	Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.80.5.2483-2494.2006}}