West Nile virus growth is independent of autophagy activation

Erica Beatman, Ryan Oyer, Katherine D. Shives, Karla Hedman, Aaron Brault, Kenneth L. Tyler, J. David Beckham

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


West Nile virus (WNV) is an arthropod-borne virus with a worldwide distribution that causes neurologic disease and death. Autophagy is a cellular homeostatic mechanism involved in antiviral responses but can be subverted to support viral growth as well. We show that autophagy is induced by WNV infection in cell culture and in primary neuron cultures. Following WNV infection, lysosomes co-localize with autophagosomes resulting in LC3B-II turnover and autolysosomal acidification. However, activation or inhibition of autophagy has no significant effect on WNV growth but pharmacologic inhibition of PI3 kinases associated with autophagy reduce WNV growth. Basal levels of p62/sequestosome1(SQSTM1) do not significantly change following WNV-induced autophagy activation, but p62 is turned over or degraded by autophagy activation implying that p62 expression is increased following WNV-infection. These data show that WNV-induces autophagy but viral growth is independent of autophagy activation suggesting that WNV-specific interactions with autophagy have diverged from other flaviviruses.

Original languageEnglish (US)
Pages (from-to)262-272
Number of pages11
Issue number1
StatePublished - Nov 10 2012
Externally publishedYes


  • Autophagy
  • Flavivirus
  • Neuron
  • P62
  • Viral encephalitis
  • West Nile virus

ASJC Scopus subject areas

  • Virology


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