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Twenty years of West Nile virus spread and evolution in the Americas visualized by Nextstrain

James Hadfield, Anderson F. Brito, Daniele M. Swetnam and 6 more

PLOS Pathogens · 2019 · Review · CC BY

doi:10.1371/journal.ppat.1008042

Abstract

It has been 20 years since West Nile virus first emerged in the Americas, and since then, little progress has been made to control outbreaks caused by this virus. After its first detection in New York in 1999, West Nile virus quickly spread across the continent, causing an epidemic of human disease and massive bird die-offs. Now the virus has become endemic to the United States, where an estimated 7 million human infections have occurred, making it the leading mosquito-borne virus infection and the most common cause of viral encephalitis in the country. To bring new attention to one of the most important mosquito-borne viruses in the Americas, we provide an interactive review using Nextstrain: a visualization tool for real-time tracking of pathogen evolution (nextstrain.org/WNV/NA). Nextstrain utilizes a growing database of more than 2,000 West Nile virus genomes and harnesses the power of phylogenetics for students, educators, public health workers, and researchers to visualize key aspects of virus spread and evolution. Using Nextstrain, we use virus genomics to investigate the emergence of West Nile virus in the U S, followed by its rapid spread, evolution in a new environment, establishment of endemic transmission, and subsequent international spread. For each figure, we include a link to Nextstrain to allow the readers to directly interact with and explore the underlying data in new ways. We also provide a brief online narrative that parallels this review to further explain the data and highlight key epidemiological and evolutionary features (nextstrain.org/narratives/twenty-years-of-WNV). Mirroring the dynamic nature of outbreaks, the Nextstrain links provided within this paper are constantly updated as new West Nile virus genomes are shared publicly, helping to stay current with the research. Overall, our review showcases how genomics can track West Nile virus spread and evolution, as well as potentially uncover novel targeted control measures to help alleviate its public health burden.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 27, 2026. Paragraph numbers are ours, so an answer can point at one.

Background

West Nile virus (WNV; family Flaviviridae; genus Flavivirus) is globally distributed and maintained by a complex transmission cycle involving multiple species of mosquitoes and birds. Since its emergence in the Americas in 1999, the virus has resulted in over 48,000 reported cases, 24,000 reported neuroinvasive cases, over 2,300 deaths, and an estimated 7 million total human infections in the continental US. At present, WNV is considered one of the most important zoonotic diseases of concern to the US population. WNV is also a significant animal pathogen, having caused over 28,000 reported equine cases and mortality in over 300 bird species, resulting in massive population declines reported among at least 23 bird species. This includes a reported 45% decline in the American Crow (Corvus brachyrhynchos) population following the introduction of WNV. The impact of WNV has not been limited to the US, as more than 5,000 human infections have been reported in Canada, and the virus is recognized as an emerging threat across the Americas.

In the two decades since WNV became established in the US, limited progress has been made in controlling transmission of the virus. Thus, renewed investment in understanding the fundamental aspects of endemic WNV transmission and innovative research directions are needed to mitigate the public health burden of WNV for the next 20 years. For example, advances in virus sequencing and phylogenetic analysis (comparing genetic variation over space and time) have transformed our ability to map the spread and evolution of viruses. Such “genomic epidemiology” approaches, for example, were recently deployed to reconstruct the emergence of Zika virus in the Americas and revealed the sources causing the yellow fever outbreaks in Brazil. For WNV, virus genomics played a central role in uncovering how the virus emerged and became endemic in a new region after its introduction in the US (e.g.,), and more detailed studies may identify transmission networks and source areas of potential reemergence to be targeted during future interventions. While powerful, these phylogenetic tools require technical expertise and computing resources that make them out of reach for some groups. To fill this need, Nextstrain (nextstrain.org) was created to provide everyone the ability to explore pathogen spread and evolution using genomic epidemiology. In this review, we use Nextstrain to uncover key epidemiological and evolutionary processes during the emergence and establishment of WNV in the Americas (nextstrain.org/WNV/NA) and discuss collaborative opportunities to advance this work for future outbreak control.

Visualizing spread and evolution using Nextstrain

Nextstrain (nextstrain.org) is an open-source initiative to use pathogen genome data to provide a real-time interactive view of the spread and evolution of significant human pathogens. The concept was born from a large collaborative project to track influenza virus evolution using rapid virus sequencing and data sharing. This aided the seasonal influenza vaccine selection process by identifying emerging virus strains that may have evolved resistance to previous vaccines. Moreover, recent epidemics of Zika and Ebola have highlighted the need for not only real-time virus genome sequencing but also rapid dissemination of epidemiologically relevant results. Thus, Nextstrain was created to provide a publicly accessible and up-to-date overview of pathogen spread and evolution during outbreaks, facilitated through collaborations with subject matter experts. Alongside platforms such as Virological (virological.org), Nextstrain has become an important venue to quickly disseminate prepublication results, which is especially critical when the information can lead to public health interventions or improved public understanding.

Nextstrain is powered by a collection of open-source bioinformatic tools to curate, analyze, and visualize available virus genomes. These datasets are used to reconstruct the geographic structure and estimated virus spread using incorporated phylogenetic tools. To reduce runtimes, Nextstrain leverages TreeTime for the maximum likelihood phylogenetic analysis, through which the entire WNV dataset currently presented on Nextstrain (n = 2,267 genomes as of June 2019) can be analyzed in under an hour on a modern computer.

We created a WNV Nextstrain resource in 2018 to convey the history of WNV in the Americas and promote new research directions (nextstrain.org/WNV/NA; S1 Fig). All of the figures herein were created using Nextstrain and contain live display links in each legend to allow the reader to explore the data. The analysis presented on Nextstrain can be recreated using our build pipeline found at github.com/grubaughlab/WNV-nextstrain, which can be used to analyze any WNV dataset offline. Additionally, we designed a new narrative function in Nextstrain to accompany this review—accessible at nextstrain.org/narratives/twenty-years-of-WNV—which walks users through the epidemiological findings discussed here in a more condensed and interactive format. Mirroring the dynamic nature of such research, Nextstrain is constantly updated as new WNV genomes are shared publicly. Thus, the live display links will always contain the most up-to-date information, helping the readers stay current with the research.

Emergence of an exotic virus

During the summer of 1999, New York City experienced a remarkably high mortality among crows and several exotic captive birds, including Chilean flamingos (Phoenicopterus chilensis) in the Bronx Zoo. Meanwhile, health professionals in Queens observed an unusual peak of unexplained human encephalitis cases, but the connection was not initially made with the increased bird mortality. Early serological investigations pointed to Saint Louis encephalitis virus (SLEV), a mosquito-borne flavivirus endemic to the Americas, as the causative agent of the human encephalitis cases. Electron microscopy investigation of viruses isolated from bird tissues also revealed flavivirus-like particles. However, SLEV is usually not associated with mortality in birds, triggering further investigation of a possible link between the virus causing encephalitis in birds and humans. Sequencing of viruses from bird and human tissues ultimately revealed that the 1999 outbreak was not caused by SLEV but, rather, a virus that had never before been observed in the Americas—WNV.

WNV was first isolated in Uganda in 1937 and has since become endemic to many parts of Africa, Europe, Asia, Australia, and the Middle East. Despite its global distribution, WNV was not detected in the Americas before the outbreak in 1999, raising two important questions: (1) where did the virus originate from and (2) when was it first introduced? Phylogenetic comparisons of the virus sequences isolated from New York in 1999 to WNV sequences from around the world revealed that it was most closely related to a WNV isolate from the brain of a dead goose found in Israel in 1998, suggesting a potential origin from the Middle East (Fig 1). Further genetic studies revealed that WNV was likely introduced in 1998 (Fig 1). Thus, WNV may have been circulating in the US for a year before the first outbreak was detected during the summer of 1999.

A still unsettled question is how the virus was brought into the US. The primary mechanism by which dengue and Zika viruses spread around the world is the long-distance travel of infected humans (e.g.,). However, unlike these viruses, WNV is maintained in a transmission cycle between birds and mosquitoes, in which humans are considered “dead-end” hosts (i.e., do not contribute to the cycle). Therefore, mobility of infected birds or mosquitoes, rather than infected humans, is the more plausible mechanism for the introduction of WNV from the Middle East into the US. While migratory birds might be important dispersers of WNV worldwide, flyways between the Middle East and North America are not common. A more likely scenario is commercial or unintentional human transportation of birds and/or mosquitoes. Mosquitoes are notorious hitchhikers on airplanes, making an introduction via one of the two international airports located within the area of the 1999 New York City WNV outbreak a plausible hypothesis. Although it is impossible to determine exactly how WNV was introduced, more detailed future investigations into the patterns of WNV introductions worldwide may reveal new insights.

Conquering a continent

Following the initial outbreak in New York in 1999, surveillance of mosquitoes and birds showed WNV spread along the eastern seaboard reaching Florida by 2001 and west to the Rocky Mountains and Pacific Northwest (Washington state) by 2002. Finally, in 2003, WNV was detected in Southern California, marking its successful establishment across the continental US.

The virus genomic data reveal that WNV spread even faster across the US than the surveillance data show (Fig 2). When combining spatial and phylogenetic data, it is estimated that the WNV “wave” moved from the East Coast to the West Coast at an average dispersal velocity of approximately 1,000 km/year during the first few years (1999–2003). Moreover, by the time WNV was first detected in New York, the virus had already spread to neighboring states (Fig 2A), before reaching parts of the Midwest and Southeast by 2000 (Fig 2B). These data also suggest that WNV was established in Texas by 2001 (Fig 2C) and California by 2002 (Fig 2D), a year before it was detected by local surveillance systems. The rapid geographical expansion of WNV between 2001 and 2002 is consistent with a large increase in virus genetic diversity (i.e., a “polytomy,” as a result of many new transmission chains being introduced; Fig 1A) and a significant jump in human cases (66 human cases in 2001 to 4,156 in 2002).

During the initial rapid spread of WNV in the US, the lack of geographic structure (i.e., “bush-like’ tree topology; S2 Fig) detected from the numerous national and regional phylogenetic studies suggests that WNV encountered a highly conducive environment with few barriers after it was introduced. This is likely due in part to the large diversity of hosts and vectors that WNV can utilize for transmission. Among these, highly abundant passerine birds (e.g., thrushes and sparrows) and Culex mosquitoes (e.g., C. tarsalis and C. pipiens) are the most important for maintaining WNV transmission. Therefore, it is likely that a large population of susceptible hosts and vectors already present in the Americas helped WNV to quickly conquer a continent despite the varied landscapes that it needed to traverse.

While the typical home ranges of residential birds and mosquitoes may account for a large portion of WNV dispersal, the rapid rates of spread, nonuniform diffusion pattern, and lack of geographical structure are best explained by frequent mixing of local and nonlocal viruses. Laboratory, field, and phylogenetic studies support the hypothesis that the introduction of nonlocal viruses was facilitated by the movement of WNV-infected migratory birds. Indeed, the early spread of WNV along the eastern seaboard aligns with a major bird migration flyway; and while the routes primarily run north and south, the elliptical migration patterns of passerines may account for the East to West WNV expansion. However, it is also possible that other mechanisms may account for the rapid spread and frequent virus mixing. For example, the impact of human behavior on WNV spread, specifically through the unintentional transport of WNV-infected birds or mosquitoes via the dense trucking industry in North America, should be examined more thoroughly. Better understanding of how WNV spreads long distances may be critical to inform future mitigation strategies.

Aided by evolution?

While WNV continues to diversify, the direct role that evolution played during the emergence of WNV in the Americas is currently difficult to discern. Evolution of WNV and other mosquito-borne viruses is complicated due to their requirement to maintain fitness in alternating and quite disparate mosquito vectors and vertebrate hosts. As a result, the WNV evolutionary rate (approximately 4 × 10 −4 substitutions/site/year; S3 Fig) is slower than many other single-host RNA viruses; and little evidence for positive selection in the virus population has been detected since the emergence of WNV in the Americas. Yet, the displacement of initial WNV genotype (termed NY99) by locally derived genotypes (WN02 and SW03) suggests that the virus may have undergone adaptive evolution in the US (Fig 3).

The defining feature of the NY99 genotype displacement is a single amino acid substitution in the WNV envelope protein (E-V159A) that emerged around 2001 (Fig 3A). By 2003, the WN02 genotype containing the E-V159A substitution became dominant (Fig 3A), corresponding to the westward spread of the virus (Fig 3B and 3C). Experimental studies have shown that compared to NY99 strains, WN02 strains may be more efficiently transmitted by C. pipiens and C. tarsalis mosquitoes and produce higher viremias during infection of house sparrows (Passer domesticus). Other studies, however, have not found differences in mosquito transmission rates between the genotypes and evidence for selection of this allele was not found during phylogenetic or experimental evolution studies. Thus, the events leading to the extinction of NY99, either by stochastic processes or through an unknown selective disadvantage, remain unknown.

Soon after the emergence of WN02 in 2001, a southwest genotype (SW03), defined by two amino acid substitutions NS4A-A85T and NS5-K314R, arose from within this clade (Fig 3A). Both of these substitutions have occurred independently multiple times (S4 Fig) and appear to be under positive selection. WN02 and SW03 continue to coexist within the US (Fig 3) and even cocirculate within the same locations, years, and mosquito vectors (e.g., Arizona, California, and New York; S5 Fig), suggesting that there are not any major barriers segregating these genotypes. However, there is some evidence that SW03 has a more rapid rate of spread than WN02 in California. This could suggest that NS4A-A85T and/or NS5-K314R are the result of recent adaptations; however, the direct fitness of either allele has yet to be experimentally evaluated. Altogether, the evidence that supports the hypothesis that rapid evolution of WNV facilitated its westwardly spread is limited, and additional studies are required to tease apart if locally derived genotypes, such as WN02 and SW03, are specifically adapted to the environment in the Americas.

Becoming an entrenched virus

Following its emergence, WNV quickly established endemicity and became one of the most important mosquito-borne viruses in North America. Since 2002, between 662 (in 2009) and 9,438 (in 2003) human WNV cases have been reported every year in the US. Evidence for endemicity from the genomic data is clear in New York, with some local transmission chains (i.e., branches on the phylogenetic tree) persisting for at least 10 years (S6 Fig). Likely due to the constant repopulation of susceptible mosquito vectors and avian hosts, the data indicate that WNV poses as an annual public health threat with no signs of remission.

Though WNV transmission is consistently detected throughout the continental US, its burden is not uniform, with a large variation in year-to-year human cases and the highest incidence rates often occurring in the central great plains (e.g., Wyoming, South Dakota, and North Dakota). Dynamic extrinsic factors, such as rainfall and temperature, that influence mosquito and bird populations can be predictive of WNV intensity, yet the contributions of these extrinsic factors vary across the US due to differences in regional ecology. This is supported by the nonuniform abundance of C. tarsalis, C. pipiens, and C. quinquefasciatus across the US, where the presence or absence of these primary mosquito vectors in a given location is mediated by many factors including human land use, elevation, and winter temperatures. Together, these ecological differences create unique transmission networks at the local and regional levels that can significantly influence the likelihood of human disease risks. These ecological barriers may further influence mosquito genetic diversity, causing potential differences in their efficiency for WNV transmission. Combined with varied avian ecology and migratory bird flyways across the US, these data suggest that WNV is maintained in regional transmission networks with unique selective pressures that influence the stability and emergence of new WNV strains.

The slowed dispersal velocity and formation of geographical segregation (S2 Fig, S6 Fig) after the initial rapid spread stage (Fig 2) reinforce the hypothesis that WNV is now primarily maintained at local or regional levels with less long-distance mixing. However, it is unclear if dynamic clustering of the virus across the US will lead to the emergence of new adaptive genotypes and if locally adapted viruses are more likely to cause outbreaks. Understanding such fundamental questions of the epidemiology and biology of WNV strains between and within states may be important for effectively combating this entrenched virus.

An international concern

The spread of WNV north to Canada and as far south as Argentina highlights that the growing burden of WNV is not limited to the US. The first human WNV case in Canada was reported in Ontario in 2002, and it has now become endemic in several southern Canadian provinces. Surveillance between 2001 and 2004 showed that WNV had spread to Central America and the Caribbean. Since then, evidence of WNV transmission has been found across South America, including Colombia, Venezuela, Brazil, and Argentina. Detection of WNV antibodies in migratory birds suggests that this route may be an important factor for WNV dissemination throughout the Americas; but as described above, it is still unclear if other mechanisms may influence the spread of WNV to Central and South America.

Although many partial WNV genomes (primarily envelope coding sequences) were generated from the Americas outside of the US (e.g.,), complete or near-complete virus genomes are necessary to accurately reconstruct spread and outbreak dynamics. To this end, there are currently only 11 WNV genomes available from Mexico, seven from the rest of Latin America and the Caribbean, and none from Canada. These limited data do reveal that the southwards spread into Latin America and the Caribbean began during the early stages of the outbreak in the US and occurred independently multiple times (Fig 4). In Mexico, multiple introductions of the WN02 and SW03 genotypes suggest that viruses may be commonly moving across the US–Mexico border. Moreover, WNV genetic data from the British Virgin Islands and Puerto Rico (partial sequences) reveal that at least the WN02 genotype was introduced into the Caribbean. Interestingly, the NY99 genotype that was displaced in the US (Fig 3) was detected in Colombia, Argentina, and Brazil, likely via separate introductions, and may still be in circulation in South America. However, the paucity of complete WNV genomes makes it difficult to understand the patterns of spread and diversity outside of the US.

An important question is why large human WNV outbreaks have not been detected in Latin American countries. The tropical and subtropical regions of the Americas have suitable conditions for the establishment of WNV, including warm temperatures, diverse avian populations, and a variety of Culex mosquitoes. Moreover, SLEV, a similar flavivirus maintained by Culex vectors and avian hosts is endemic throughout the Americas. Considering that the “old” NY99 genotype virus was recently detected in Brazil and serological evidence of WNV is prevalent in resident birds from Latin America, it is likely that WNV is endemic throughout the Americas. Perhaps the presence of other mosquito-borne viruses has thus far masked human cases (e.g., misdiagnosed as dengue) or may convey some level of cross-protection. Alternatively, as WNV may have initially outcompeted SLEV in the US, the presence of competitive SLEV genotypes in Central and South America may have at least temporarily slowed WNV transmission in these regions. Given these uncertainties, initiatives to introduce human and equine serosurveys and dead bird and mosquito surveillance for WNV in regions throughout the Americas are paramount for determining its true burden.

Future role of genomics

Given how much WNV has thrived in the US, significant national investment will be required to control future outbreaks. Among this investment should include sustained and collaborative efforts to fill in the many gaps in WNV genomic sampling throughout the country, especially from the last 10 years (Fig 5), to better understand endemic WNV transmission using virus genomics approaches. Fortunately, the availability of scalable, easy, and relatively inexpensive sequencing tools (e.g.,) make these efforts more achievable, and recent work by Swetnam and colleagues, Hepp and colleagues, Bialosuknia and colleagues, and the WestNile 4K Project (westnile4k.org/) provides a template for future public health and academic lab partnerships. Platforms such as Nextstrain (nextstrain.org/WNV/NA) and Virological (virological.org) allow these new data to be continually communicated to the public.

Generating a well-distributed temporal and spatial WNV genomic dataset can be used to determine which strains are causing outbreaks and, importantly, where those strains came from and when they became locally established. This work will help to identify if WNV outbreaks in Ames, Iowa, for example, are connected to outbreaks as far away as Des Moines, Iowa (approximately 60 km); Omaha, Nebraska (approximately 270 km); or even Chicago, Illinois (approximately 560 km). Systematically searching for connections among WNV outbreaks around the country may reveal endemic “transmission networks,” which could be exploited for control and forecasting purposes. WNV control is primarily based on local interventions to temporarily reduce the populations of mosquito vectors, but the long-term effects are likely limited by recolonization of mosquitoes and reintroductions of viruses once the pressure is removed. Thus, a highly coordinated effort among several health departments and mosquito abatement districts to synchronize vector control within a transmission network may reduce reintroductions and limit WNV transmission beyond a single season. In addition, genomic epidemiology approaches with large-scale efforts to collect and share mosquito abundance and infection rate data may help to identify potential patterns of virus outbreaks (e.g., as used to identify factors contributing to the Ebola epidemic). This, in turn, could be used to maximize vector control efforts by strategically focusing resources at a precise time and location to limit potential outbreaks. After 20 years of WNV in the Americas, it is time to recognize that alleviating the burden of WNV for the next generation will likely depend on significant investment, new approaches, and large collaborations.

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    May FJ, Davis CT, Tesh RB, Barrett ADT. Phylogeography of West Nile virus: From the cradle of evolution in Africa to Eurasia, Australia, and the Americas. J Virol. 2011;85: 2964–2974.

    Not in our library10.1128/jvi.01963-10

  43. 43.

    Zehender G, Ebranati E, Bernini F, Lo Presti A, Rezza G, Delogu M, et al Phylogeography and epidemiological history of West Nile virus genotype 1a in Europe and the Mediterranean basin. Infection, Genetics and Evolution. 2011;11: 646–653.

    Not in our library10.1016/j.meegid.2011.02.003

  44. 44.

    Johnston BL, Conly JM. West Nile virus—where did it come from and where might it go? Canadian Journal of Infectious Diseases. 2000;11: 175–178.

    Not in our library10.1155/2000/856598

  45. 45.

    Tian H, Sun Z, Faria NR, Yang J, Cazelles B, Huang S, et al Increasing airline travel may facilitate co-circulation of multiple dengue virus serotypes in Asia. PLoS Negl Trop Dis. 2017;11: e0005694

    Not in our library10.1371/journal.pntd.0005694

  46. 46.

    Viana DS, Santamaría L, Figuerola J. Migratory birds as global dispersal vectors. Trends Ecol Evol. 2016;31: 763–775.

    Not in our library10.1016/j.tree.2016.07.005

  47. 47.
    Emergence of West Nile Virus Lineage 2 in Europe: A Review on the Introduction and Spread of a Mosquito-Borne Disease · 2014
    No notice
  48. 48.

    Reed KD, Meece JK, Henkel JS, Shukla SK. Birds, migration and emerging zoonoses: West Nile virus, Lyme disease, influenza A and enteropathogens. Clin Med Res. 2003;1: 5–12.

    Not in our library10.3121/cmr.1.1.5

  49. 49.

    CDC. West Nile Virus Activity—United States, September 26-October 2, 2002, and Investigations of West Nile Virus Infections in Recipients of Blood Transfusion and Organ Transplantation [Internet]. 23 Oct 2002. Available from: https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5139a5.htm. [cited 2019 May 5].

    Not in our library

  50. 50.
    West Nile Virus in California · 2004
    No notice
  51. 51.

    Beasley DWC, Davis CT, Guzman H, Vanlandingham DL, Travassos da Rosa APA, Parsons RE, et al Limited evolution of West Nile virus has occurred during its southwesterly spread in the United States. Virology. 2003;309: 190–195.

    Not in our library10.1016/s0042-6822(03)00150-8

  52. 52.

    Herring BL, Bernardin F, Caglioti S, Stramer S, Tobler L, Andrews W, et al Phylogenetic analysis of WNV in North American blood donors during the 2003–2004 epidemic seasons. Virology. 2007;363: 220–228.

    Not in our library10.1016/j.virol.2007.01.019

  53. 53.

    Grinev A, Chancey C, Volkova E, Añez G, Heisey DAR, Winkelman V, et al Genetic variability of West Nile virus in US blood donors from the 2012 epidemic season. PLoS Negl Trop Dis. 2016;10: e0004717

    Not in our library10.1371/journal.pntd.0004717

  54. 54.

    Anez G, Grinev A, Chancey C, Ball C, Akolkar N, Land KJ, et al Evolutionary dynamics of West Nile virus in the United States, 1999–2011: Phylogeny, selection pressure and evolutionary time-scale analysis. PLoS Negl Trop Dis. 2013;7: e2245

    Not in our library10.1371/journal.pntd.0002245

  55. 55.

    Davis CT, Beasley DWC, Guzman H, Raj R, D’Anton M, Novak RJ, et al Genetic variation among temporally and geographically distinct West Nile virus isolates, United States, 2001, 2002. Emerg Infect Dis. 2003;9: 1423–1429.

    Not in our library10.3201/eid0911.030301

  56. 56.

    Bertolotti L, Kitron UD, Walker ED, Ruiz MO, Brawn JD, Loss SR, et al Fine-scale genetic variation and evolution of West Nile Virus in a transmission “hot spot” in suburban Chicago, USA. Virology. 2008;374: 381–389.

    Not in our library10.1016/j.virol.2007.12.040

  57. 57.

    Amore G, Bertolotti L, Hamer GL, Kitron UD, Walker ED, Ruiz MO, et al Multi-year evolutionary dynamics of West Nile virus in suburban Chicago, USA, 2005–2007. Philos Trans R Soc Lond B Biol Sci. 2010;365: 1871–1878.

    Not in our library10.1098/rstb.2010.0054

  58. 58.

    Bertolotti L, Kitron U, Goldberg TL. Diversity and evolution of West Nile virus in Illinois and the United States, 2002–2005. Virology. 2007;360: 143–149.

    Not in our library10.1016/j.virol.2006.10.030

  59. 59.
    Experimental Infection of North American Birds with the New York 1999 Strain of West Nile Virus · 2003
    No notice
  60. 60.

    Turell MJ, O’Guinn M, Oliver J. Potential for New York mosquitoes to transmit West Nile virus. Am J Trop Med Hyg. 2000;62: 413–414.

    Not in our library10.4269/ajtmh.2000.62.413

  61. 61.
    Vector Competence of California Mosquitoes for West Nile virus · 2002
    No notice
  62. 62.
    Vector Competence of Selected North American Culex and Coquillettidia Mosquitoes for West Nile Virus · 2001
    No notice
  63. 63.

    Rappole JH, Compton BW, Leimgruber P, Robertson J, King DI, Renner SC. Modeling movement of West Nile virus in the western hemisphere. Vector Borne Zoonotic Dis. 2006;6: 128–139.

    Not in our library10.1089/vbz.2006.6.128

  64. 64.

    Venkatesan M, Rasgon JL. Population genetic data suggest a role for mosquito-mediated dispersal of West Nile virus across the western United States. Mol Ecol. 2010;19: 1573–1584.

    Not in our library10.1111/j.1365-294x.2010.04577.x

  65. 65.

    Owen J, Moore F, Panella N, Edwards E, Bru R, Hughes M, et al Migrating birds as dispersal vehicles for West Nile virus. Ecohealth. 2006;3: 79.

    Not in our library

  66. 66.

    Dusek RJ, McLean RG, Kramer LD, Ubico SR, Dupuis AP 2nd, Ebel GD, et al Prevalence of West Nile virus in migratory birds during spring and fall migration. Am J Trop Med Hyg. 2009;81: 1151–1158.

    Not in our library10.4269/ajtmh.2009.09-0106

  67. 67.

    Reisen WK, Wheeler SS, Garcia S, Fang Y. Migratory birds and the dispersal of arboviruses in California. Am J Trop Med Hyg. 2010;83: 808–815.

    Not in our library10.4269/ajtmh.2010.10-0200

  68. 68.

    Rappole JH, Derrickson SR, Hubálek Z. Migratory birds and spread of West Nile virus in the western hemisphere. Emerg Infect Dis. 2000;6: 319–328.

    Not in our library10.3201/eid0604.000401

  69. 69.

    Weaver SC, Rico-Hesse R, Scott TW. Genetic diversity and slow rates of evolution in New World alphaviruses. Current Topics in Microbiology and Immunology. 1992; 99–117.

    Not in our library10.1007/978-3-642-77011-1_7

  70. 70.

    Weaver SC, Brault AC, Kang W, Holland JJ. Genetic and fitness changes accompanying adaptation of an arbovirus to vertebrate and invertebrate cells. J Virol. 1999;73: 4316–4326.

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  71. 71.

    Ciota AT, Lovelace AO, Ngo KA, Le AN, Maffei JG, Franke MA, et al Cell-specific adaptation of two flaviviruses following serial passage in mosquito cell culture. Virology. 2007;357: 165–174.

    Not in our library10.1016/j.virol.2006.08.005

  72. 72.

    Grubaugh ND, Fauver JR, Ruckert C, Weger-Lucarelli J, Garcia-Luna S, Murrieta RA, et al Mosquitoes transmit unique West Nile virus populations during each feeding episode. Cell Rep. 2017;19: 709–718.

    Not in our library10.1016/j.celrep.2017.03.076

  73. 73.

    Deardorff ER, Fitzpatrick KA, Jerzak GVS, Shi P-Y, Kramer LD, Ebel GD. West Nile virus experimental evolution in vivo and the trade-off hypothesis. PLoS Pathog. 2011;7: e1002335

    Not in our library10.1371/journal.ppat.1002335

  74. 74.

    Jenkins GM, Rambaut A, Pybus OG, Holmes EC. Rates of molecular evolution in RNA viruses: A quantitative phylogenetic analysis. J Mol Evol. 2002;54: 156–165.

    Not in our library10.1007/s00239-001-0064-3

  75. 75.

    Granwehr BP, Li L, Davis CT, Beasley DWC, Barrett ADT. Characterization of a West Nile virus isolate from a human on the Gulf Coast of Texas. J Clin Microbiol. 2004;42: 5375–5377.

    Not in our library10.1128/jcm.42.11.5375-5377.2004

  76. 76.

    Ebel GD, Carricaburu J, Young D, Bernard KA, Kramer LD. Genetic and phenotypic variation of West Nile virus in New York, 2000–2003. Am J Trop Med Hyg. 2004;71: 493–500.

    Not in our library

  77. 77.

    Moudy RM, Meola MA, Morin L-LL, Ebel GD, Kramer LD. A newly emergent genotype of West Nile virus is transmitted earlier and more efficiently by Culex mosquitoes. Am J Trop Med Hyg. 2007;77: 365–370.

    Not in our library

  78. 78.
    Temperature, Viral Genetics, and the Transmission of West Nile Virus by Culex pipiens Mosquitoes · 2008
    No notice
  79. 79.

    Duggal NK, Bosco-Lauth A, Bowen RA, Wheeler SS, Reisen WK, Felix TA, et al Evidence for co-evolution of West Nile virus and house sparrows in North America. PLoS Negl Trop Dis. 2014;8: e3262

    Not in our library10.1371/journal.pntd.0003262

  80. 80.

    Anderson JF, Main AJ, Cheng G, Ferrandino FJ, Fikrig E. Horizontal and vertical transmission of West Nile virus genotype NY99 by Culex salinarius and genotypes NY99 and WN02 by Culex tarsalis. Am J Trop Med Hyg. 2012;86: 134–139.

    Not in our library10.4269/ajtmh.2012.11-0473

  81. 81.

    Vanlandingham DL, McGee CE, Klingler KA, Galbraith SE, Barrett ADT, Higgs S. Short report: Comparison of oral infectious dose of West Nile virus isolates representing three distinct genotypes in Culex quinquefasciatus. Am J Trop Med Hyg. 2008;79: 951–954.

    Not in our library

  82. 82.

    Danforth ME, Reisen WK, Barker CM. Extrinsic incubation rate is not accelerated in recent California strains of West Nile virus in Culex tarsalis (Diptera: Culicidae). J Med Entomol. 2015;52: 1083–1089.

    Not in our library10.1093/jme/tjv082

  83. 83.

    Grubaugh ND, Smith DR, Brackney DE, Bosco-Lauth AM, Fauver JR, Campbell CL, et al Experimental evolution of an RNA virus in wild birds: Evidence for host-dependent impacts on population structure and competitive fitness. PLoS Pathog. 2015;11: e1004874

    Not in our library10.1371/journal.ppat.1004874

  84. 84.

    Grubaugh ND, Weger-Lucarelli J, Murrieta RA, Fauver JR, Garcia-Luna SM, Prasad AN, et al Genetic drift during systemic arbovirus infection of mosquito vectors leads to decreased relative fitness during host switching. Cell Host Microbe. 2016;19: 481–492.

    Not in our library10.1016/j.chom.2016.03.002

  85. 85.

    McMullen AR, May FJ, Li L, Guzman H, Bueno R Jr, Dennett JA, et al Evolution of new genotype of West Nile virus in North America. Emerg Infect Dis. 2011;17: 785–793.

    Not in our library10.3201/eid1705.101707

  86. 86.

    Añez G, Grinev A, Chancey C, Ball C, Akolkar N, Land KJ, et al Evolutionary dynamics of West Nile virus in the United States, 1999–2011: Phylogeny, selection pressure and evolutionary time-scale analysis. PLoS Negl Trop Dis. 2013;7: e2245

    Not in our library10.1371/journal.pntd.0002245

  87. 87.

    Bialosuknia SM, Tan Y, Zink SD, Koetzner CA, Maffei JG, Halpin RA, et al Evolutionary dynamics and molecular epidemiology of West Nile virus in New York State: 1999–2015. Virus Evol. 2019;5: vez020

    Not in our library10.1093/ve/vez020

  88. 88.

    Paull SH, Horton DE, Ashfaq M, Rastogi D, Kramer LD, Diffenbaugh NS, et al Drought and immunity determine the intensity of West Nile virus epidemics and climate change impacts. Proceedings of the Royal Society B. 2017;

    Not in our library10.1098/rspb.2016.2078

  89. 89.

    Landesman WJ, Allan BF, Langerhans RB, Knight TM, Chase JM. Inter-annual associations between precipitation and human incidence of West Nile virus in the United States. Vector Borne Zoonotic Dis. 2007;7

    Not in our library10.1089/vbz.2006.0590

  90. 90.

    Shaman J, Day JF, Stieglitz M. Drought-induced amplification and epidemic transmission of West Nile virus in southern Florida. J Med Entomol. 2005;42: 134–141.

    Not in our library10.1093/jmedent/42.2.134

  91. 91.

    Wimberly MC, Lamsal A, Giacomo P, Chuang TW. Regional variation of climatic influences on West Nile virus outbreaks in the United States. Am J Trop Med Hyg. 2014;91: 677–684.

    Not in our library10.4269/ajtmh.14-0239

  92. 92.
    Local impact of temperature and precipitation on West Nile virus infection in Culex species mosquitoes in northeast Illinois, USA · 2010
    No notice
  93. 93.

    Davis JK, Vincent G, Hildreth MB, Kightlinger L, Carlson C, Wimberly MC. Integrating environmental monitoring and mosquito surveillance to predict vector-borne disease: Prospective forecasts of a West Nile virus outbreak. PLoS Curr. 2017;

    Not in our library10.1371/currents.outbreaks.90e80717c4e67e1a830f17feeaaf85de

  94. 94.

    Chuang TW, Wimberly MC. Remote sensing of climatic anomalies and West Nile virus incidence in the northern great plains of the United States. PLoS ONE. 2012;7: 1–10.

    Not in our library10.1371/journal.pone.0046882

  95. 95.
    Vector-Virus Interactions and Transmission Dynamics of West Nile Virus · 2013
    No notice
  96. 96.

    Kilpatrick AM. Globalization, land use, and the invasion of West Nile virus. Science. 2011;334: 323–327.

    Not in our library10.1126/science.1201010

  97. 97.

    Dunphy BM, Kovach KB, Gehrke EJ, Field EN, Rowley WA, Bartholomay LC, et al Long-term surveillance defines spatial and temporal patterns implicating Culex tarsalis as the primary vector of West Nile virus. Sci Rep. 2019;9: 6637

    Not in our library10.1038/s41598-019-43246-y

  98. 98.

    Andreadis TG. The contribution of Culex pipiens complex mosquitoes to transmission and persistence of West Nile virus in North America. Journal of American Mosquito Control Association. 2012;28: 137–151.

    Not in our library10.2987/8756-971x-28.4s.137

  99. 99.

    Gibbs SEJ, Wimberly MC, Madden M, Masour J, Yabsley MJ, Stallknecht DE. Factors affecting the geographic distribution of West Nile virus in Georgia, USA: 2002–2004. Vector Borne Zoonotic Dis. 2006;6: 73–82.

    Not in our library10.1089/vbz.2006.6.73

  100. 100.

    Bowden SE, Magori K, Drake JM. Regional differences in the association between land cover and West Nile virus disease incidence in humans in the United States. Am J Trop Med Hyg. 2011;84: 234–238.

    Not in our library10.4269/ajtmh.2011.10-0134

  101. 101.

    Kothera L, Godsey MS, Doyle MS, Savage HM. Characterization of Culex pipiens complex (Diptera: Culicidae) populations in Colorado, USA using microsatellites. PLoS ONE. 2012;7: 1–9.

    Not in our library10.1371/journal.pone.0047602

  102. 102.

    Ciota AT, Chin PA, Kramer LD. The effect of hybridization of Culex pipiens complex mosquitoes on transmission of West Nile virus. Parasit Vectors. 2013;6: 305

    Not in our library10.1186/1756-3305-6-305

  103. 103.

    Giordano BV, Kaur S, Hunter FF. West Nile virus in Ontario, Canada: A twelve-year analysis of human case prevalence, mosquito surveillance, and climate data. PLoS ONE. 2017;12: e0183568

    Not in our library10.1371/journal.pone.0183568

  104. 104.

    Dupuis AP 2nd, Marra PP, Kramer LD. Serologic evidence of West Nile virus transmission, Jamaica, West Indies. Emerg Infect Dis. 2003;9: 860–863.

    Not in our library10.3201/eid0907.030249

  105. 105.
    West Nile Virus in Mexico: Evidence of Widespread Circulation since July 2002. · 2003
    Not checked
  106. 106.

    Komar N, Clark GG. West Nile virus activity in Latin America and the Caribbean. Revista Panamericana de Salud Pública. 2006;19: 112–117.

    Not in our library10.1590/s1020-49892006000200006

  107. 107.

    Elizondo-Quiroga D, Davis CT, Fernandez-Salas I, Escobar-Lopez R, Velasco Olmos D, Soto Gastalum LC, et al West Nile Virus isolation in human and mosquitoes, Mexico. Emerg Infect Dis. 2005;11: 1449–1452.

    Not in our library10.3201/eid1109.050121

  108. 108.

    Mattar S, Edwards E, Laguado J, González M, Alvarez J, Komar N. West Nile virus antibodies in Colombian horses. Emerg Infect Dis. 2005;11: 1497–1498.

    Not in our library10.3201/eid1109.050426

  109. 109.
    West Nile Virus Isolation from Equines in Argentina, 2006 · 2006
    No notice
  110. 110.

    Bosch I, Herrera F, Navarro J-C, Lentino M, Dupuis A, Maffei J, et al West Nile virus, Venezuela. Emerg Infect Dis. 2007;13: 651–653.

    Not in our library10.3201/eid1304.061383

  111. 111.

    Pauvolid-Corrêa A, Morales MA, Levis S, Figueiredo LTM, Couto-Lima D, Campos Z, et al Neutralising antibodies for West Nile virus in horses from Brazilian Pantanal. Mem Inst Oswaldo Cruz. 2011;106: 467–474.

    Not in our library10.1590/s0074-02762011000400014

  112. 112.

    Ulloa A, Ferguson HH, Méndez-Sánchez JD, Danis-Lozano R, Casas-Martínez M, Bond JG, et al West Nile virus activity in mosquitoes and domestic animals in Chiapas, México. Vector Borne Zoonotic Dis. 2009;9: 555–560.

    Not in our library10.1089/vbz.2008.0087

  113. 113.

    Dudas G, Bedford T. The ability of single genes vs full genomes to resolve time and space in outbreak analysis [Internet]. bioRxiv. 2019 p. 582957

    Not in our library10.1101/582957

  114. 114.

    Mann BR, McMullen AR, Guzman H, Tesh RB, Barrett ADT. Dynamic transmission of West Nile virus across the United States-Mexican border. Virology. 2013;436: 75–80.

    Not in our library10.1016/j.virol.2012.10.023

  115. 115.

    Deardorff E, Estrada-Franco J, Brault AC, Navarro-Lopez R, Campomanes-Cortes A, Paz-Ramirez P, et al Introductions of West Nile virus strains to Mexico. Emerg Infect Dis. 2006;12: 314–318.

    Not in our library10.3201/eid1202.050871

  116. 116.

    Osorio JE, Ciuoderis KA, Lopera JG, Piedrahita LD, Murphy D, Levasseur J, et al Characterization of West Nile viruses isolated from captive American flamingoes (Phoenicopterus ruber) in Medellin, Colombia. Am J Trop Med Hyg. 2012;87: 565–572.

    Not in our library10.4269/ajtmh.2012.11-0655

  117. 117.

    Fabbri CM, García JB, Morales MA, Enría DA, Levis S, Lanciotti RS. Complete genome sequences and phylogenetic analysis of two West Nile virus strains isolated from equines in Argentina in 2006 could indicate an early introduction of the virus in the Southern Cone. Vector Borne Zoonotic Dis. 2014;14: 794–800.

    Not in our library10.1089/vbz.2014.1588

  118. 118.

    Martins LC, Silva EVP da, Casseb LMN, Silva SP da, Cruz ACR, Pantoja JA de S, et al First isolation of West Nile virus in Brazil. Mem Inst Oswaldo Cruz. 2019;114: e180332

    Not in our library10.1590/0074-02760180332

  119. 119.

    Anthony SJ, Garner MM, Palminteri L, Navarrete-Macias I, Sanchez-Leon MD, Briese T, et al West Nile virus in the British Virgin Islands. Ecohealth. 2014;11: 255–257.

    Not in our library10.1007/s10393-014-0910-6

  120. 120.

    Mann BR, McMullen AR, Swetnam DM, Barrett ADT. Molecular epidemiology and evolution of West Nile virus in North America. Int J Environ Res Public Health. 2013;10: 5111–5129.

    Not in our library10.3390/ijerph10105111

  121. 121.

    Barrera R, Hunsperger E, Muñoz-Jordán JL, Amador M, Diaz A, Smith J, et al First isolation of West Nile virus in the Caribbean. Am J Trop Med Hyg. 2008;78: 666–668.

    Not in our library

  122. 122.

    Gubler DJ. The continuing spread of West Nile virus in the western hemisphere. Clin Infect Dis. 2007;45: 1039–1046.

    Not in our library10.1086/521911

  123. 123.

    Kopp A, Gillespie TR, Hobelsberger D, Estrada A, Harper JM, Miller RA, et al Provenance and geographic spread of St. Louis encephalitis virus. MBio. 2013;4: e00322–13.

    Not in our library10.1128/mbio.00322-13

  124. 124.
    Reemergence of St. Louis Encephalitis Virus in the Americas · 2018
    Not checked
  125. 125.

    Quick J, Grubaugh ND, Pullan ST, Claro IM, Smith AD, Gangavarapu K, et al Multiplex PCR method for MinION and Illumina sequencing of Zika and other virus genomes directly from clinical samples. Nature Protocols. 2017;12: 1261–1276.

    Not in our library10.1038/nprot.2017.066

  126. 126.

    Metsky HC, Siddle KJ, Gladden-Young A, Qu J, Yang DK, Brehio P, et al Capturing sequence diversity in metagenomes with comprehensive and scalable probe design. Nat Biotechnol. 2019;37: 160–168.

    Not in our library10.1038/s41587-018-0006-x

  127. 127.

    Gubler DJ, Campbell GL, Nasci R, Komar N, Petersen L, Roehrig JT. West Nile virus in the United States: Guidelines for detection, prevention, and control. Viral Immunology. 2000;13: 469–475.

    Not in our library10.1089/vim.2000.13.469

  128. 128.

    Rund SSC, Martinez ME. Rescuing hidden ecological data to tackle emerging mosquito-borne diseases. Available from: https://www.biorxiv.org/content/early/2017/08/09/096875.abstract. 2017; 096875. [cited 2019 June 11].

    Not in our library10.2987/18-6781.1

  129. 129.

    Dudas G, Carvalho LM, Bedford T, Tatem AJ, Baele G, Faria NR, et al Virus genomes reveal factors that spread and sustained the Ebola epidemic. Nature. 2017;544: 309–315.

    Not in our library10.1038/nature22040

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