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J. Biol. Chem., Vol. 281, Issue 48, 37025-37033, December 1, 2006

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Trim5 Accelerates Degradation of Cytosolic Capsid Associated with Productive HIV-1 Entry^*

Udayan Chatterji, Michael D. Bobardt, Peter Gaskill, Dennis Sheeter^¶, Howard Fox, and Philippe A. Gallay¹

From the Departments of Immunology, Molecular and Integrative Neurosciences, and ^¶Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037

The TRIM5 (tripartite motif 5 protein) has been linked to the cross-species restriction in human immunodeficiency virus type 1 (HIV-1) infection of non-human cells, but the mechanism by which this occurs remains to be fully elucidated. Here we demonstrate that the capsid (CA) protein of HIV-1 is more rapidly degraded in cells expressing monkey TRIM5 than in cells expressing human TRIM5. Other proteins encoded by Gag and Pol are not subject to TRIM5-mediated accelerated degradation. The accelerated CA degradation by TRIM5 apparently occurs via a nonproteosomal pathway. TRIM5 selectively accelerates degradation of the CA population, which reached the cytosol of restrictive cells, but not the CA population, which ended into the vesicular compartment. Given that cytosolic CA represents "productively" entered cores, whereas vesicular CA represents "nonproductively" entered cores, our findings suggest that TRIM5 interrupts the infectious pathway of HIV-1 by acting on the incoming cytosolic CA. The mode of viral entry does not influence the accelerated degradation of cytosolic CA by TRIM5. Thus, this study reveals a correlation between TRIM5-mediated HIV-1 restriction and a selective degradation of cytosolic CA normally associated with productive viral entry.

Received for publication, June 26, 2006 , and in revised form, October 4, 2006.

^* This work was supported by a Center for AIDS Research developmental grant (to P. G.) from the United States Public Health Service and NIAID Grant 5 P30 AI036214 from the National Institutes of Health. This is publication number 17792 from the Department of Immunology, The Scripps Research Institute, La Jolla, CA. 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 Immunology IMM-9, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037. Tel.: 858-784-8180; Fax: 858-784-8227; E-mail: gallay{at}scripps.edu.

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