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Journal articles
Semen-mediated enhancement of HIV infection is donor-dependent and correlates with the levels of SEVI.
Abstract : BACKGROUND: HIV-1 is usually transmitted in the presence of semen. We have shown that semen boosts HIV-1 infection and contains fragments of prostatic acid phosphatase (PAP) forming amyloid aggregates termed SEVI (semen-derived enhancer of viral infection) that promote virion attachment to target cells. Despite its importance for the global spread of HIV-1, however, the effect of semen on virus infection is controversial. RESULTS: Here, we established methods allowing the meaningful analysis of semen by minimizing its cytotoxic effects and partly recapitulating the conditions encountered during sexual HIV-1 transmission. We show that semen rapidly and effectively enhances the infectivity of HIV-1, HIV-2, and SIV. This enhancement occurs independently of the viral genotype and coreceptor tropism as well as the virus producer and target cell type. Semen-mediated enhancement of HIV-1 infection was also observed under acidic pH conditions and in the presence of vaginal fluid. We further show that the potency of semen in boosting HIV-1 infection is donor dependent and correlates with the levels of SEVI. CONCLUSIONS: Our results show that semen strongly enhances the infectivity of HIV-1 and other primate lentiviruses and that SEVI contributes to this effect. Thus, SEVI may play an important role in the sexual transmission of HIV-1 and addition of SEVI inhibitors to microbicides may improve their efficacy.
https://www.hal.inserm.fr/inserm-00663892
Contributor : Ed. Bmc Connect in order to contact the contributor
Submitted on : Friday, January 27, 2012 - 5:14:25 PM
Last modification on : Thursday, January 14, 2021 - 11:19:47 AM
Long-term archiving on: : Saturday, April 28, 2012 - 2:40:33 AM
Contributor : Ed. Bmc Connect in order to contact the contributor
Submitted on : Friday, January 27, 2012 - 5:14:25 PM
Last modification on : Thursday, January 14, 2021 - 11:19:47 AM
Long-term archiving on: : Saturday, April 28, 2012 - 2:40:33 AM