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20 - Influences of arthropod vectors on encephalitic arboviruses

from Section III - Introduction: immunity, diagnosis, vector, and beneficial uses of neurotropic viruses

Published online by Cambridge University Press:  22 August 2009

Stephen Higgs
Affiliation:
Center for Biodefense & Emerging Infectious Diseases, Sealy Center for Vaccine Development and WHO Collaborating Center for Tropical Diseases, Department of Pathology, University of Texas Medical Branch, Galveston, Texas
Carol Shoshkes Reiss
Affiliation:
New York University
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Summary

Introduction

Arthropod-borne viruses (arboviruses) are found in several virus families including Bunyaviridae, Togaviridae, Flaviviridae, Orthomyxoviridae, Rhabdoviridae, and Reoviridae. Many are not pathogenic for their natural vertebrate hosts, but those that do cause disease are often associated with a broad range of clinical manifestations. For example, most human West Nile virus (WNV) infections are asymptomatic, but some progress rapidly to a fatal encephalitic outcome [1]. Although this variability can be partly correlated with host characteristics (e.g., age and immune status) interactions between the virus and the vertebrate host that lead to disease are often complex and poorly understood. For a particular arbovirus, different species of vertebrate may play different roles in the viral maintenance and transmission cycle. It is not well understood why some species are apparently genetically resistant to infection (i.e., not a host for replication) whereas others are highly susceptible (i.e., readily infected following exposure to a low viral dose). Maintenance vertebrate hosts that play a critical role in virus amplification and the infection of vectors must produce a sufficiently high titer of virus in the blood (viremia) to ensure that the recipient vector becomes infected. This is usually referred to as the infection threshold and may be accompanied by clinical symptoms such as fever, but it does not necessarily correlate with disease severity. Conversely, hosts that do not produce threshold viremic levels sufficient to infect vectors (so-called “dead-end” hosts) may succumb to infection.

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Print publication year: 2008

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  • Influences of arthropod vectors on encephalitic arboviruses
    • By Stephen Higgs, Center for Biodefense & Emerging Infectious Diseases, Sealy Center for Vaccine Development and WHO Collaborating Center for Tropical Diseases, Department of Pathology, University of Texas Medical Branch, Galveston, Texas
  • Edited by Carol Shoshkes Reiss, New York University
  • Book: Neurotropic Viral Infections
  • Online publication: 22 August 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511541728.025
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  • Influences of arthropod vectors on encephalitic arboviruses
    • By Stephen Higgs, Center for Biodefense & Emerging Infectious Diseases, Sealy Center for Vaccine Development and WHO Collaborating Center for Tropical Diseases, Department of Pathology, University of Texas Medical Branch, Galveston, Texas
  • Edited by Carol Shoshkes Reiss, New York University
  • Book: Neurotropic Viral Infections
  • Online publication: 22 August 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511541728.025
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  • Influences of arthropod vectors on encephalitic arboviruses
    • By Stephen Higgs, Center for Biodefense & Emerging Infectious Diseases, Sealy Center for Vaccine Development and WHO Collaborating Center for Tropical Diseases, Department of Pathology, University of Texas Medical Branch, Galveston, Texas
  • Edited by Carol Shoshkes Reiss, New York University
  • Book: Neurotropic Viral Infections
  • Online publication: 22 August 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511541728.025
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