Genetic Determinants of Virulence in Pathogenic Lineage 2 West Nile Virus Strains

Botha, Elizabeth C.

doi:10.3201/eid1401.070457

Cited by 41 publications

(47 citation statements)

References 17 publications

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“…A single amino acid substitution in the central portion of NS4B, C102S, was enough to attenuate neurovirulence in mice (Wicker et al, 2006). Lineage II WNV has been associated with encephalitis and more severe disease only rarely, but comparison of the strains isolated from patients with more severe disease to less virulent strains indicates an enhanced role for NS proteins in determining virulence, relative to structural proteins, similar to findings for lineage I (Botha et al, 2008). …”

Section: Genetic Correlates Of Pathogenesis and Fitnessmentioning

confidence: 89%

West Nile virus population genetics and evolution

Pesko

Ebel

2012

Infection, Genetics and Evolution

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West Nile virus (WNV) (Flaviviridae: Flavivirus) is transmitted from mosquitoes to birds, but can cause fatal encephalitis in infected humans. Since its introduction into North America in New York in 1999, it has spread throughout the western hemisphere. Multiple outbreaks have also occurred in Europe over the last 20 years. This review highlights recent efforts to understand how host pressures impact viral population genetics, genotypic and phenotypic changes which have occurred in the WNV genome as it adapts to this novel environment, and molecular epidemiology of WNV worldwide. Future research directions are also discussed.

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Section: Genetic Correlates Of Pathogenesis and Fitnessmentioning

confidence: 89%

West Nile virus population genetics and evolution

Pesko

Ebel

2012

Infection, Genetics and Evolution

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“…Thus, divergence between New and Old World HOSP populations is likely, and these experiments with North American HOSPs may not be consistent with other geographically distinct HOSP populations. Interestingly, amino acid variation at the E-159 locus has been observed in Old World Lineage 1A WNV isolates several times prior to the introduction of WNV to North America [50], as well as Lineage 2 WNV strains [51], but no other lineage has acquired an alanine at this position. Since HOSPs are prevalent in Europe and Africa and would likely serve as important avian hosts, it is possible that other substitutions at E-159 are beneficial to viral replication in distinct HOSP populations.…”

Section: Discussionmentioning

confidence: 99%

Evidence for Co-evolution of West Nile Virus and House Sparrows in North America

et al. 2014

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West Nile virus (WNV) has been maintained in North America in enzootic cycles between mosquitoes and birds since it was first described in North America in 1999. House sparrows (HOSPs; Passer domesticus) are a highly competent host for WNV that have contributed to the rapid spread of WNV across the U.S.; however, their competence has been evaluated primarily using an early WNV strain (NY99) that is no longer circulating. Herein, we report that the competence of wild HOSPs for the NY99 strain has decreased significantly over time, suggesting that HOSPs may have developed resistance to this early WNV strain. Moreover, recently isolated WNV strains generate higher peak viremias and mortality in contemporary HOSPs compared to NY99. These data indicate that opposing selective pressures in both the virus and avian host have resulted in a net increase in the level of host competence of North American HOSPs for currently circulating WNV strains.

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“…An adaptive mutation E 249 G in the same protein reduced virus replication in mouse cells ( 14 ). In lineage 2 strains, substitutions in the NS3 protein (S 160 A and R 298 G), NS4A protein (A 79 T), and NS5 protein (T 614 P, M 625 R, and M 626 R) were predicted to be possible virulence markers ( 15 ). All these foci were checked in the Nea Santa-Greece-2010 strain, but differences were not found, except for the 249 residue of the NS3 protein.…”

Section: The Studymentioning

confidence: 99%