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 journalArticle

11 Citations (Scopus)

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

Fingerprint

Autophagy
Hepacivirus
Antiviral Agents
Viral Nonstructural Proteins
Proteins
Interleukin-1 Receptors
Liver Failure
Serine Proteases
Tretinoin
Innate Immunity
Proteolysis
Immunity
Homeostasis
Fibrosis
Chronic Disease
Warfare
Carcinoma
Liver
Genes

Keywords

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

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

IFNα/β and autophagy : Tug-of-war between HCV and the host. / Sun, Jiaren; Desai, Mayura M.; Soong, Lynn; Ou, J. H James.

In: Autophagy, Vol. 7, No. 11, 11.2011, p. 1394-1396.

Research output: Contribution to journalArticle

Sun, Jiaren ; Desai, Mayura M. ; Soong, Lynn ; Ou, J. H James. / IFNα/β and autophagy : Tug-of-war between HCV and the host. In: Autophagy. 2011 ; Vol. 7, No. 11. pp. 1394-1396.
@article{29a2e283a7da4f57af2f725a2489bc6d,
title = "IFNα/β and autophagy: Tug-of-war between HCV and the host",
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.",
keywords = "Autophagy, Hepatitis C virus, Liver disease, NS3/4A protease, RIG-I, TLR3, Transgenic mouse, Type I interferon",
author = "Jiaren Sun and Desai, {Mayura M.} and Lynn Soong and Ou, {J. H James}",
year = "2011",
month = "11",
doi = "10.4161/auto.7.11.17514",
language = "English (US)",
volume = "7",
pages = "1394--1396",
journal = "Autophagy",
issn = "1554-8627",
publisher = "Landes Bioscience",
number = "11",

}

TY - JOUR

T1 - IFNα/β and autophagy

T2 - Tug-of-war between HCV and the host

AU - Sun, Jiaren

AU - Desai, Mayura M.

AU - Soong, Lynn

AU - Ou, J. H James

PY - 2011/11

Y1 - 2011/11

N2 - 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.

AB - 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.

KW - Autophagy

KW - Hepatitis C virus

KW - Liver disease

KW - NS3/4A protease

KW - RIG-I

KW - TLR3

KW - Transgenic mouse

KW - Type I interferon

UR - http://www.scopus.com/inward/record.url?scp=80655134724&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80655134724&partnerID=8YFLogxK

U2 - 10.4161/auto.7.11.17514

DO - 10.4161/auto.7.11.17514

M3 - Article

C2 - 21997372

AN - SCOPUS:80655134724

VL - 7

SP - 1394

EP - 1396

JO - Autophagy

JF - Autophagy

SN - 1554-8627

IS - 11

ER -