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Human influenza viruses activate an interferon-independent transcription of cellular antiviral genes: outcome with influenza A virus is unique.

Abstract：

:We examine the IFN-alpha/beta-independent activation of cellular transcription that constitutes an early antiviral response of cells against influenza A and B viruses, which cause widespread epidemics in humans. We show that influenza B virus induces the synthesis in human cells of several mature mRNAs encoded by genes containing an IFN-alpha/beta-stimulated response element (ISRE). Consequently, the IFN regulatory factor-3 transcription factor, which is required for the transcription of ISRE-controlled genes, is activated after influenza B virus infection. The production of these cellular mRNAs, some of which encode antiviral proteins, is independent of not only IFN-alpha/beta, but also viral protein synthesis. These mature cellular antiviral mRNAs are not produced after infection with influenza A virus, but IFN regulatory factor-3 is activated and the transcription of the ISRE-controlled p56 gene is induced. Consequently, like other newly synthesized cellular premRNAs in influenza A virus-infected cells, the posttranscriptional processing of premRNAs encoded by ISRE-controlled genes is inhibited. Previous work has established that such posttranscriptional inhibition is mediated by the viral NS1A protein. This unique, global countermeasure against the early, IFN-alpha/beta-independent antiviral response of cells may be an important factor in the pathogenicity of influenza A virus infection.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Kim MJ,Latham AG,Krug RM

doi

10.1073/pnas.152327499

keywords:

subject

Has Abstract

pub_date

2002-07-23 00:00:00

pages

10096-101

issue

15

eissn

0027-8424

issn

1091-6490

pii

152327499

journal_volume

99

pub_type

杂志文章

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