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J. Biol. Chem., Vol. 283, Issue 25, 16966-16970, June 20, 2008

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Cytomegalovirus M45 Cell Death Suppression Requires Receptor-interacting Protein (RIP) Homotypic Interaction Motif (RHIM)-dependent Interaction with RIP1^*

From the Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322

Herpesviruses such as cytomegaloviruses encode functions that modulate the innate response in diverse ways to counteract host sensing and delay host clearance during infection. The murine cytomegalovirus M45 protein interacts with receptor-interacting protein (RIP) 1 and RIP3 via a RIP homotypic interaction motif. Cell death suppression by M45 requires RIP homotypic interaction motif-dependent interaction with RIP1. This interaction also underlies the cell tropism role of M45 in preventing premature death of endothelial cells during murine cytomegalovirus infection. Thus, M45 is a viral inhibitor of RIP activation that provides a direct cell type-dependent replication benefit to the virus while modulating other biological processes signaling via the RIP1 adaptor such as activation of Toll-like receptor (TLR)3 as well as other mediators of cell death.

Received for publication, March 4, 2008 , and in revised form, April 18, 2008.

^* This work was supported, in whole or in part, by National Institutes of Health Grants RO1 AI 030363 (to E. S. M.) and T32 HL069769 (to J. W. U.) from the USPHS. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Microbiology and Immunology, Emory Vaccine Center, 1462 Clifton Rd. NE, Emory University School of Medicine, Atlanta GA 30322. Tel.: 404-727-9442; Fax: 404-712-9736; E-mail: mocarski{at}emory.edu.

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