Pathogenesis of flavivirus encephalitis

Within the flavivirus family, viruses that cause natural infections of the central nervous system (CNS) principally include members of the Japanese encephalitis virus (JEV) serogroup and the tick-borne encephalitis virus (TBEV) serocomplex. The pathogenesis of diseases involves complex interactions...

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Published inAdvances in Virus Research Vol. 60; pp. 273 - 342
Main Authors Chambers, Thomas J, Diamond, Michael S
Format Book Chapter Journal Article
LanguageEnglish
Published United States Elsevier Science & Technology 2003
Elsevier Inc
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Abstract Within the flavivirus family, viruses that cause natural infections of the central nervous system (CNS) principally include members of the Japanese encephalitis virus (JEV) serogroup and the tick-borne encephalitis virus (TBEV) serocomplex. The pathogenesis of diseases involves complex interactions of viruses, which differ in neurovirulence potential, and a number of host factors, which govern susceptibility to infection and the capacity to mount effective antiviral immune responses both in the periphery and within the CNS. This chapter summarizes progress in the field of flavivirus neuropathogenesis. Mosquito-borne and tickborne viruses are considered together. Flavivirus neuropathogenesis involves both neuroinvasiveness (capacity to enter the CNS) and neurovirulence (replication within the CNS), both of which can be manipulated experimentally. Neuronal injury as a result of bystander effects may be a factor during flavivirus neuropathogenesis given that microglial activation and elaboration of inflammatory mediators, including IL-1β and TNF-α, occur in the CNS during these infections and may accompany the production of nitric oxide and peroxynitrite, which can cause neurotoxicity.
AbstractList Within the flavivirus family, viruses that cause natural infections of the central nervous system (CNS) principally include members of the Japanese encephalitis virus (JEV) serogroup and the tick-borne encephalitis virus (TBEV) serocomplex. The pathogenesis of diseases involves complex interactions of viruses, which differ in neurovirulence potential, and a number of host factors, which govern susceptibility to infection and the capacity to mount effective antiviral immune responses both in the periphery and within the CNS. This chapter summarizes progress in the field of flavivirus neuropathogenesis. Mosquito-borne and tickborne viruses are considered together. Flavivirus neuropathogenesis involves both neuroinvasiveness (capacity to enter the CNS) and neurovirulence (replication within the CNS), both of which can be manipulated experimentally. Neuronal injury as a result of bystander effects may be a factor during flavivirus neuropathogenesis given that microglial activation and elaboration of inflammatory mediators, including IL-1β and TNF-α, occur in the CNS during these infections and may accompany the production of nitric oxide and peroxynitrite, which can cause neurotoxicity.
Author Diamond, Michael S
Chambers, Thomas J
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  surname: Diamond
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  organization: Department of Molecular Microbiology, Medicine, Pathology, and Immunology Washington University School of Medicine St. Louis, Missouri 63110, USA
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SubjectTerms Animals
Brain - pathology
Brain - virology
Complement System Proteins - physiology
Encephalitis, Arbovirus - etiology
Encephalitis, Arbovirus - immunology
Encephalitis, Tick-Borne - etiology
Encephalitis, Tick-Borne - immunology
Flavivirus
Flavivirus - pathogenicity
Flavivirus Infections - etiology
Flavivirus Infections - immunology
Humans
Immunology
Interferon-gamma - biosynthesis
Killer Cells, Natural - immunology
Macrophages - immunology
Virology
West Nile virus - pathogenicity
Title Pathogenesis of flavivirus encephalitis
URI https://dx.doi.org/10.1016/S0065-3527(03)60008-4
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Volume 60
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