Wild type and H43Y variant of human TRIM5α show similar anti-human immunodeficiency virus type 1 activity both in vivo and in vitro
Polymorphisms in human genes have been shown to affect the rate of disease progression to acquired immune deficiency syndrome in human immunodeficiency virus type 1 (HIV-1)-infected individuals. Recently, tripartite motif 5α (TRIM5α) was identified as a factor that confers resistance to HIV-1 infection in Old World monkey cells. Subsequently, Sawyer et al. (Curr Biol 16:95–100, 2006) reported a single nucleotide polymorphism (H43Y) in the human TRIM5α gene and TRIM5α protein with 43Y was found to lose its ability to restrict HIV-1. In the present study, we reevaluated effects of this allele on in vitro anti-HIV-1 activity as well as on HIV-1 disease progression in European and Asian cohorts of HIV-1-infected individuals. Our epidemiological and molecular biological findings clearly indicate H43Y has a very minor effect on anti-HIV-1 activity of TRIM5α, suggesting that this allele is immaterial, at least in HIV-1-infected Europeans and Asians.
KeywordsTRIM5α H43Y RING domain Polymorphism HIV-1 disease progression Anti-HIV-1 activity
- Javanbakht H, An P, Gold B, Petersen DC, O’Huigin C, Nelson GW, O’Brien SJ, Kirk GD, Detels R, Buchbinder S, Donfield S, Shulenin S, Song B, Perron MJ, Stremlau M, Sodroski J, Dean M, Winkler C (2006) Effects of human TRIM5alpha polymorphisms on antiretroviral function and susceptibility to human immunodeficiency virus infection. Virology 354:15–27PubMedCrossRefGoogle Scholar
- Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL (2005) Harrison’s Principles of Internal Medicine. McGraw-Hill, New YorkGoogle Scholar