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Journal of Virology, April 2005, p. 3930-3937, Vol. 79, No. 7
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.7.3930-3937.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Retrovirus Restriction by TRIM5
Variants from Old World and New World Primates
Byeongwoon Song,1
Hassan Javanbakht,1
Michel Perron,1
Do Hyun Park,1
Matthew Stremlau,1 and
Joseph Sodroski1,2*
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Department of Pathology, Division of AIDS, Harvard Medical School,1
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts2
Received 9 September 2004/
Accepted 3 November 2004
The TRIM5
proteins of humans and some Old World monkeys have been shown to block infection of particular retroviruses following virus entry into the host cell. Infection of most New World monkey cells by the simian immunodeficiency virus of macaques (SIVmac) is restricted at a similar point. Here we examine the antiretroviral activity of TRIM5
orthologs from humans, apes, Old World monkeys, and New World monkeys. Chimpanzee and orangutan TRIM5
proteins functionally resembled human TRIM5
, potently restricting infection by N-tropic murine leukemia virus (N-MLV) and moderately restricting human immunodeficiency virus type 1 (HIV-1) infection. Notably, TRIM5
proteins from several New World monkey species restricted infection by SIVmac and the SIV of African green monkeys, SIVagm. Spider monkey TRIM5
, which has an expanded B30.2 domain v3 region due to a tandem triplication, potently blocked infection by a range of retroviruses, including SIVmac, SIVagm, HIV-1, and N-MLV. Tandem duplications in the TRIM5
B30.2 domain v1 region of African green monkeys are also associated with broader antiretroviral activity. Thus, variation in TRIM5
proteins among primate species accounts for the observed patterns of postentry restrictions in cells from these animals. The TRIM5
proteins of some monkey species exhibit dramatic lengthening of particular B30.2 variable regions and an expanded range of susceptible retroviruses.
* Corresponding author. Mailing address: Dana-Farber Cancer Institute, 44 Binney St., JFB 824, Boston, MA 02115. Phone: (617) 632-3371. Fax: (617) 632-4338. E-mail:
joseph_sodroski{at}dfci.harvard.edu.
Journal of Virology, April 2005, p. 3930-3937, Vol. 79, No. 7
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.7.3930-3937.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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