Introductions of West Nile Virus Strains to Mexico

Deardorff, Eleanor R.; Estrada-Franco, José G.; Brault, Aaron C.; Navarro-Lopez, Roberto; Campomanes-Cortes, Arturo; Paz-Ramirez, Pedro; Solís-Hernández, Mario; Ramey, Wanichaya N.; Davis, C. Todd; Beasley, David W.C.; Tesh, Robert B.; Barrett, Alan D.T.; Weaver, Scott C.

doi:10.3201/eid1202.050871

Cited by 63 publications

(71 citation statements)

References 16 publications

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“…10,[32][33][34][35][36][37][38] Despite this fact, with the exception of sites adjacent to the United States border, 39 WNV was isolated only once in Mexico from a diseased raven in a Tabasco zoo. 11 This paucity of viral isolations could be the result of a combination of reduced avian mortality, reduced viral loads within avian hosts, or limited mosquito testing.…”

Section: Discussionmentioning

confidence: 99%

Reduced Avian Virulence and Viremia of West Nile Virus Isolates from Mexico and Texas

Brault¹,

Langevin

Ramey

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Abstract. A West Nile virus (WNV) isolate from Mexico (TM171-03) and BIRD1153, a unique genotype from Texas, have exhibited reduced murine neuroinvasive phenotypes. To determine if murine neuroinvasive capacity equates to avian virulence potential, American crow ( Corvus brachyrhynchos ) and house sparrows ( Passer domesticus ) were experimentally inoculated with representative murine neuroinvasive/non-neuroinvasive strains. In both avian species, a plaque variant from Mexico that was E-glycosylation competent produced higher viremias than an E-glycosylation-incompetent variant, indicating the potential importance of E-glycosylation for avian replication. The murine non-neuroinvasive BIRD1153 strain was significantly attenuated in American crows but not house sparrows when compared with the murine neuroinvasive Texas strain. Despite the loss of murine neuroinvasive properties of nonglycosylated variants from Mexico, our data indicate avian replication potential of these strains and that unique WNV virulence characteristics exist between murine and avian models. The implications of reduced avian replication of variants from Mexico for restricted WNV transmission in Latin America is discussed.

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Section: Discussionmentioning

confidence: 99%

Reduced Avian Virulence and Viremia of West Nile Virus Isolates from Mexico and Texas

Brault¹,

Langevin

Ramey

et al. 2011

The American Society of Tropical Medicine and Hygiene

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“…It is not only maintained in an enzootic cycle between mosquitoes and birds [4], but can also infect and cause disease in other vertebrates including mice. After its discovery in the USA in 1999, WNV spread rapidly across North America, and also has been reported in Central and South America [5][6][7]. Between 1999 and 2010, there were a total of 1.8 million human illnesses, 1308 of which resulted in death [8].…”

Section: Introductionmentioning

confidence: 99%

Estimating biologically relevant parameters under uncertainty for experimental within-host murine West Nile virus infection

Banerjee

Guedj

Ribeiro

et al. 2016

J. R. Soc. Interface.

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West Nile virus (WNV) is an emerging pathogen that has decimated bird populations and caused severe outbreaks of viral encephalitis in humans. Currently, little is known about the within-host viral kinetics of WNV during infection. We developed mathematical models to describe viral replication, spread and host immune response in wild-type and immunocompromised mice. Our approach fits a target cell-limited model to viremia data from immunocompromised knockout mice and an adaptive immune response model to data from wild-type mice. Using this approach, we first estimate parameters governing viral production and viral spread in the host using simple models without immune responses. We then use these parameters in a more complex immune response model to characterize the dynamics of the humoral immune response. Despite substantial uncertainty in input parameters, our analysis generates relatively precise estimates of important viral characteristics that are composed of nonlinear combinations of model parameters: we estimate the mean within-host basic reproductive number, R 0 , to be 2.3 (95% of values in the range 1.7-2.9); the mean infectious virion burst size to be 2.9 plaqueforming units (95% of values in the range 1.7-4.7); and the average number of cells infected per infectious virion to be between 0.3 and 0.99. Our analysis gives mechanistic insights into the dynamics of WNV infection and produces estimates of viral characteristics that are difficult to measure experimentally. These models are a first step towards a quantitative understanding of the timing and effectiveness of the humoral immune response in reducing host viremia and consequently the epidemic spread of WNV.

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“…The virus can cause febrile illness and neurologic disease in a range of avian and mammalian hosts, including humans. Since its introduction to North America in 1999 in the New York City area (Lanciotti et al 1999), WNV spread rapidly throughout the United States, Canada (Gancz et al 2004), Mexico (Deardorff et al 2006) and Latin America and the Caribbean as far south as Argentina (Petersen & Hayes 2008). Now endemic in the Americas, WNV is transmitted in different geographical regions by local species of Culex.…”

Section: Introductionmentioning

confidence: 99%

Multi-year evolutionary dynamics of West Nile virus in suburban Chicago, USA, 2005–2007

Amore

Bertolotti

Hamer

et al. 2010

Phil. Trans. R. Soc. B

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West Nile virus has evolved in concert with its expansion across North America, but little is known about the evolutionary dynamics of the virus on local scales. We analysed viral nucleotide sequences from mosquitoes collected in 2005, 2006, and 2007 from a known transmission 'hot spot' in suburban Chicago, USA. Within this approximately 11 Â 14 km area, the viral envelope gene has increased approximately 0.1% yr 21 in nucleotide-level genetic diversity. In each year, viral diversity was higher in 'residential' sites characterized by dense housing than in more open 'urban green space' sites such as cemeteries and parks. Phylodynamic analyses showed an increase in incidence around 2005, consistent with a higher-than-average peak in mosquito and human infection rates that year. Analyses of times to most recent common ancestor suggest that WNV in 2005 and 2006 may have arisen predominantly from viruses present during 2004 and 2005, respectively, but that WNV in 2007 had an older common ancestor, perhaps indicating a predominantly mixed or exogenous origin. These results show that the population of WNV in suburban Chicago is an admixture of viruses that are both locally derived and introduced from elsewhere, containing evolutionary information aggregated across a breadth of spatial and temporal scales.

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Introductions of West Nile Virus Strains to Mexico

Cited by 63 publications

References 16 publications

Reduced Avian Virulence and Viremia of West Nile Virus Isolates from Mexico and Texas

Reduced Avian Virulence and Viremia of West Nile Virus Isolates from Mexico and Texas

Estimating biologically relevant parameters under uncertainty for experimental within-host murine West Nile virus infection

Multi-year evolutionary dynamics of West Nile virus in suburban Chicago, USA, 2005–2007

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