Published April 25, 2007 | Version v1
Journal article

Group 2 coronaviruses prevent immediate early interferon induction by protection of viral RNA from host cell recognition

  • 1. Molecular Virology Laboratory, Department of Medical Microbiology, Center of Infectious Diseases, Leiden University Medical Center, LUMC E4-P, P.O. Box 9600, 2300 RC Leiden (Netherlands)

Description

Many viruses encode antagonists to prevent interferon (IFN) induction. Infection of fibroblasts with the murine hepatitis coronavirus (MHV) and SARS-coronavirus (SARS-CoV) did not result in nuclear translocation of interferon-regulatory factor 3 (IRF3), a key transcription factor involved in IFN induction, and induction of IFN mRNA transcription. Furthermore, MHV and SARS-CoV infection could not prevent IFN induction by poly (I:C) or Sendai virus, suggesting that these CoVs do not inactivate IRF3-mediated transcription regulation, but apparently prevent detection of replicative RNA by cellular sensory molecules. Our data indicate that shielding of viral RNA to host cell sensors might be the main general mechanism for coronaviruses to prevent IFN induction

Additional details

Identifiers

DOI
10.1016/j.virol.2007.01.020;
PII
S0042-6822(07)00044-X;

Publishing Information

Journal Title
Virology
Journal Volume
361
Journal Issue
1
Journal Page Range
p. 18-26
ISSN
0042-6822
CODEN
VIRLAX

INIS

Country of Publication
United States
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
39006836
Subject category
S60: APPLIED LIFE SCIENCES;
Descriptors DEI
FIBROBLASTS; GENE REGULATION; HEPATITIS; INTERFERON; RNA; SHIELDING; TRANSCRIPTION; TRANSCRIPTION FACTORS; TRANSLOCATION; VIRUSES
Descriptors DEC
ANIMAL CELLS; CONNECTIVE TISSUE CELLS; DIGESTIVE SYSTEM DISEASES; DISEASES; GROWTH FACTORS; LYMPHOKINES; MICROORGANISMS; MITOGENS; NUCLEIC ACIDS; ORGANIC COMPOUNDS; PARASITES; PROTEINS; SOMATIC CELLS

Optional Information

Copyright
Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.