Apoptosis in alphavirus encephalitis

Research output: Contribution to journalArticle

Abstract

Sindbis virus causes acute encephalitis in mice and serves as a useful model for encephalitic alphaviruses that infect humans. The outcome of infection is determined by whether infected neurons are resistant to virus-induced programmed cell death or activate their apoptotic pathway. The host immune response may also cause death of infected neurons. Determinants of neuronal apoptosis include the maturity of the neuron, the virulence of the infecting virus and the cellular immune response to infection. In many situations viral and cellular factors that decrease virus replication also decrease apoptosis. Antiviral antibody can downregulate virus replication in surviving neurons without affecting cell viability. Other innate and induced host immune responses can alter the outcome of infection without a change in virus production. Failure to induce apoptosis in infected neurons leads to long-term persistence of small amounts of viral RNA in the nervous system of infected mice despite the clearance of infectious virus. The molecular mechanisms that govern these pathogenesis factors are beginning to be elucidated.

Original languageEnglish (US)
Pages (from-to)481-489
Number of pages9
JournalSeminars in Virology
Volume8
Issue number6
DOIs
StatePublished - Aug 1998

Fingerprint

Alphavirus
Encephalitis
Apoptosis
Neurons
Viruses
Virus Replication
Infection
Sindbis Virus
Viral RNA
Cellular Immunity
Nervous System
Antiviral Agents
Virulence
Cause of Death
Cell Survival
Cell Death
Down-Regulation
Antibodies

ASJC Scopus subject areas

  • Immunology
  • Virology

Cite this

Apoptosis in alphavirus encephalitis. / Griffin, Diane; Hardwick, J Marie.

In: Seminars in Virology, Vol. 8, No. 6, 08.1998, p. 481-489.

Research output: Contribution to journalArticle

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