IFNα/β and autophagy: Tug-of-war between HCV and the host

Jiaren Sun, Mayura M. Desai, Lynn Soong, J. H.James Ou

Research output: Contribution to journalShort survey

13 Scopus citations

Abstract

Hepatitis C virus (HCV) infects approximately 130 million people worldwide. The clinical sequelae of this chronic disease include cirrhosis, functional failure and carcinoma of the liver. HCV induces autophagy, a fundamental cellular process for maintaining homeostasis and mediating innate immune response, and also inhibits autophagic protein degradation and suppresses antiviral immunity. In addition to this ploy, the HCV serine protease composed of the viral nonstructural proteins 3/4A (NS3/4A) can enzymatically digest two cellular proteins, mitochondriaassociated antiviral signaling protein (MAVS) and toll/interleukin-1 receptor domain containing adaptor inducing IFNβ (TRIF). Since these two proteins are the adaptor molecules in the retinoic acid-inducible gene I (RIG-I) and TLR3 pathways, respectively, their cleavage has been suggested as a pivotal mechanism by which HCV blunts the IFNα/β signaling and antiviral responses. Thus far, how HCV perturbs autophagy and copes with IFNα/β in the liver remains unclear.

Original languageEnglish (US)
Pages (from-to)1394-1396
Number of pages3
JournalAutophagy
Volume7
Issue number11
DOIs
StatePublished - Nov 2011

Keywords

  • Autophagy
  • Hepatitis C virus
  • Liver disease
  • NS3/4A protease
  • RIG-I
  • TLR3
  • Transgenic mouse
  • Type I interferon

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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