Research
Semen-mediated enhancement of HIV infection is donor-dependent and correlates with the levels of SEVI
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* Corresponding authors: Frank Kirchhoff frank.kirchhoff@uni-ulm.de - Jan Münch jan.muench@uni-ulm.de
- † Equal contributors
1 Institute of Molecular Virology, University Hospital Ulm, 89081 Ulm, Germany
2 Gladstone Institute of Virology and Immunology, University of California, San Francisco, CA 94158, USA
3 Peptide Research Group, Clinic for Immunology, Hannover Medical School, Hannover, Germany
4 VIRO Pharmaceuticals GmbH & Co. KG, Hannover, Germany
5 National Laboratory for HIV Immunology, Public Health Agency of Canada, Winnipeg, Manitoba, R3E 3P6, Canada
6 INSERM U625, Rennes; Rennes University, Groupe d'Etude de la Reproduction chez l'Homme et les Mammifères; IFR 140, Campus de Beaulieu, Rennes, France
7 Departments of Medicine and Microbiology, University of Alabama at Birmingham, Birmingham, AL 35223, USA
Retrovirology 2010, 7:55 doi:10.1186/1742-4690-7-55
Published: 23 June 2010Abstract
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.