Abstract

West Nile virus (WNV; Flavivirus; Flaviviridae) is the cause of the most widespread arthropod-borne viral disease in the world and the largest outbreak of neuroinvasive disease ever observed. Mosquito-borne outbreaks are influenced by intrinsic (e.g., vector and viral genetics, vector and host competence, vector life-history traits) and extrinsic (e.g., temperature, rainfall, human land use) factors that affect virus activity and mosquito biology in complex ways. The concept of vectorial capacity integrates these factors to address interactions of the virus with the arthropod host, leading to a clearer understanding of their complex interrelationships, how they affect transmission of vector-borne disease, and how they impact human health. Vertebrate factors including host competence, population dynamics, and immune status also affect transmission dynamics. The complexity of these interactions are further exacerbated by the fact that not only can divergent hosts differentially alter the virus, but the virus also can affect both vertebrate and invertebrate hosts in ways that significantly alter patterns of virus transmission. This chapter concentrates on selected components of the virus-vector-vertebrate interrelationship, focusing specifically on how interactions between vector, virus, and environment shape the patterns and intensity of WNV transmission.

Highlights

  • West Nile virus (WNV; Flaviviridae; Flavivirus) was first detected in the Americas in 1999, the result of a single point introduction into the New York City area [1,2], followed by a dramatic range expansion [3,4,5,6]

  • Species distribution and population density suggest that Culex pipiens L. and Culex restuans Theobald may be responsible for up to 80% of human WNV infections in the northeastern United States (USA) [12]

  • Cx. tarsalis is not known to hybridize, yet significant spatial genetic clustering is noted [38,39], which likely contributes to population level variability in vectorial capacity

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Summary

Introduction

West Nile virus (WNV; Flaviviridae; Flavivirus) was first detected in the Americas in 1999, the result of a single point introduction into the New York City area [1,2], followed by a dramatic range expansion [3,4,5,6]. Extrinsic factors influence contact between the mosquito and susceptible vertebrate hosts and include such elements as density and composition of the host and vector populations, and environmental conditions. These factors together contribute to selective pressures shaping dynamic viral populations, host-virus outcomes and, epidemiological patterns. We review current knowledge of the dynamic and complex nature of factors influencing WNV vectorial capacity, as well as how these factors broadly impact vertebrate host infections and competence

Vector Distribution and Genetics
Vectorial Capacity
WNV Infection and Mosquito Life History Traits
Mosquito Immunity and Microbial Interactions
Vertebrate
Avian Host Competence
Other Vertebrates
Population Genetics and Molecular Epidemiology
Bottlenecks and Intrahost Diversity
Adaptive Constraint
Findings
Concluding Remarks
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