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Am J Reprod Immunol. 2011 Feb;65(2):89-98. doi: 10.1111/j.1600-0897.2010.00902.x.

Innate immunity and inflammatory response to Trichomonas vaginalis and bacterial vaginosis: relationship to HIV acquisition.

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  • 1Department of Obstetrics and Gynecology, CONRAD Clinical Research Center and CONRAD Microbicide Research Laboratory, Eastern Virginia Medical School, Norfolk, VA 23507, USA.


Most women contract HIV-1 through sexual intercourse with an infected partner. Highly prevalent, unreported and often asymptomatic lower genital tract infections, including bacterial vaginosis (BV) and trichomoniasis (Trichomonas vaginalis- TV), increase a woman's susceptibility to HIV-1 genital infection, given an exposure. A review of the literature from 1989 to the present was conducted. This article will review potential mechanisms by which BV and TV serve as HIV-1-enhancing cofactors including (i) initiation of a clinical or subclinical mucosal inflammatory response, (ii) alteration of innate mucosal immunity, (iii) alteration of normal vaginal microflora and pH, and (iv) weakening or breach of intact cervico-vaginal mucosa. The transmission of HIV-1, in the absence of cofactors, is poorly efficient. Understanding the mechanisms by which these infections enhance HIV-1 acquisition is important to designing effective, safe and evidence-based prevention modalities.

© 2010 John Wiley & Sons A/S.

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