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Journal of Virology, July 2005, p. 8969-8978, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8969-8978.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Human Tripartite Motif 5{alpha} Domains Responsible for Retrovirus Restriction Activity and Specificity

David Perez-Caballero,{dagger} Theodora Hatziioannou,{dagger} Annie Yang, Simone Cowan, and Paul D. Bieniasz*

Aaron Diamond AIDS Research Center and the Rockefeller University, New York, New York 10016

Received 4 February 2005/ Accepted 26 March 2005

The tripartite motif 5{alpha} protein (TRIM5{alpha}) is one of several factors expressed by mammalian cells that inhibit retrovirus replication. Human TRIM5{alpha} (huTRIM5{alpha}) inhibits infection by N-tropic murine leukemia virus (N-MLV) but is inactive against human immunodeficiency virus type 1 (HIV-1). However, we show that replacement of a small segment in the carboxy-terminal B30.2/SPRY domain of huTRIM5{alpha} with its rhesus macaque counterpart (rhTRIM5{alpha}) endows it with the ability to potently inhibit HIV-1 infection. The B30.2/SPRY domain and an additional domain in huTRIM5{alpha}, comprising the amino-terminal RING and B-box components of the TRIM motif, are required for N-MLV restriction activity, while the intervening coiled-coil domain is necessary and sufficient for huTRIM5{alpha} multimerization. Truncated huTRIM5{alpha} proteins that lack either or both the N-terminal RING/B-Box or the C-terminal B30.2/SPRY domain form heteromultimers with full-length huTRIM5{alpha} and are dominant inhibitors of its N-MLV restricting activity, suggesting that homomultimerization of intact huTRIM5{alpha} monomers is necessary for N-MLV restriction. However, localization in large cytoplasmic bodies is not required for inhibition of N-MLV by huTRIM5{alpha} or for inhibition of HIV-1 by chimeric or rhTRIM5{alpha}.

* Corresponding author. Mailing address: Aaron Diamond AIDS Research Center, 455 First Ave., New York, NY 10021. Phone: (212) 448-5070. Fax: (212) 725-1126. E-mail: pbienias{at}adarc.org.

{dagger} P.-C. and T.H. contributed equally to this study.

Journal of Virology, July 2005, p. 8969-8978, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8969-8978.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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