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PMID: 15994826 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Respiratory syncytial virus nonstructural proteins NS1 and NS2 mediate inhibition of Stat2 expression and alpha/beta interferon responsiveness.

Journal of virology ·Vol. 79 ·No. 14 ·2005-07-00 ·Pages 9315-9

Lo MS, Brazas RM, Holtzman MJ

Abstract

Respiratory syncytial virus (RSV) subverts the antiviral interferon (IFN) response, but the mechanism for this evasion was unclear. Here we show that RSV preferentially inhibits IFN-alpha/beta signaling by expression of viral NS1 and NS2. Thus, RSV infection or expression of recombinant NS1 and NS2 in epithelial host cells causes a marked decrease in Stat2 levels and the consequent downstream IFN-alpha/beta response. Similarly, NS1/NS2-deficient RSV no longer decreases Stat2 levels or IFN responsiveness. RSV infection decreased human but not mouse Stat2 levels, so this mechanism of IFN antagonism may contribute to viral host range, as well as immune subversion.

MeSH Terms
Cell Line DNA-Binding Proteins/analysis,antagonists & inhibitors Humans Interferon-alpha/antagonists & inhibitors Interferon-beta/antagonists & inhibitors Respiratory Syncytial Virus Infections/immunology Respiratory Syncytial Virus, Human/physiology STAT2 Transcription Factor Signal Transduction Trans-Activators/analysis,antagonists & inhibitors Viral Nonstructural Proteins/physiology
Chemicals
DNA-Binding Proteins Interferon-alpha STAT2 Transcription Factor STAT2 protein, human Trans-Activators Viral Nonstructural Proteins Interferon-beta
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Lo Mindy S
Department of Medicine, Washington University School of Medicine, Campus Box 8052, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Brazas Robert M
Holtzman Michael J
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
2005-07-00
Pages
9315-9
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC1168759
Subset
IM
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