NDLI: A46R and A52R from vaccinia virus are antagonists of host IL-1 and toll-like receptor signaling

Content Provider	PubMed Central
Author	Bowie, Andrew Endre, Kiss-toth Symons, Julian A. Smith, Geoffrey L. Dower, Steven K. O'neill, Luke A. J.
Copyright Year	2000
Abstract	Poxviruses employ many strategies to evade and neutralize the host immune response. In this study, we have identified two vaccinia virus ORFs, termed A46R and A52R, that share amino acid sequence similarity with the Toll/IL-1 receptor (TIR) domain, a motif that defines the IL-1/Toll-like receptor (TLR) superfamily of receptors, which have a key role in innate immunity and inflammation. When expressed in mammalian cells, the protein products of both ORFs were shown to interfere specifically with IL-1 signal transduction. A46R partially inhibited IL-1-mediated activation of the transcription factor NFκB, and A52R potently blocked both IL-1- and TLR4-mediated NFκB activation. MyD88 is a TIR domain-containing adapter molecule known to have a central role in both IL-1 and TLR4 signaling. A52R mimicked the dominant-negative effect of a truncated version of MyD88 on IL-1, TLR4, and IL-18 signaling but had no effect on MyD88-independent signaling pathways. Therefore, A46R and A52R are likely to represent a mechanism used by vaccinia virus of suppressing TIR domain-dependent intracellular signaling.
Related Links	http://dx.doi.org/10.1073/pnas.160027697
Ending Page	10167
Page Count	6
Starting Page	10162
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	18
Volume Number	97
Language	English
Publisher	The National Academy of Sciences
Publisher Date	2000-08-29
Access Restriction	Open
Rights Holder	The National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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A46R and A52R from vaccinia virus are antagonists of host IL-1 and toll-like receptor signaling