Autophagy and viral neurovirulence

Anthony Orvedahl, Beth Levine

Research output: Contribution to journalShort survey

60 Scopus citations

Abstract

As terminally differentiated vital cells, neurons may be specialized to fight viral infections without undergoing cellular self-destruction. The cellular lysosomal degradation pathway, autophagy, is emerging as one such mechanism of neuronal antiviral defence. Autophagy has diverse physiological functions, such as cellular adaptation to stress, routine organelle and protein turnover, and innate immunity against intracellular pathogens, including viruses. Most of the in vivo evidence for an antiviral role of autophagy is related to viruses that specifically target neurons, including the prototype alphavirus, Sindbis virus, and the α-herpesvirus, herpes simplex virus type 1 (HSV-1). In the case of HSV-1, viral evasion of autophagy is essential for lethal encephalitis. As basal autophagy is important in preventing neurodegeneration, and induced autophagy is important in promoting cellular survival during stress, viral antagonism of autophagy in neurons may lead to neuronal dysfunction and/or neuronal cell death. This review provides background information on the roles of autophagy in immunity and neuroprotection, and then discusses the relationships between autophagy and viral neurovirulence.

Original languageEnglish (US)
Pages (from-to)1747-1756
Number of pages10
JournalCellular Microbiology
Volume10
Issue number9
DOIs
StatePublished - Aug 11 2008

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Virology

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