Innate Immunity and Inflammatory Response to Trichomonas vaginalis and Bacterial Vaginosis: Relationship to HIV Acquisition

Authors

  • Andrea R. Thurman,

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

    1. Department of Obstetrics and Gynecology, CONRAD Clinical Research Center and CONRAD Microbicide Research Laboratory, Eastern Virginia Medical School, Norfolk, VA, USA
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Andrea R. Thurman, MD, Associate Professor of Obstetrics and Gynecology, CONRAD Clinical Research Center, Eastern Virginia Medical School, 601 Colley Avenue, Norfolk, VA 23507, USA.
E-mail: thurmaar@evms.edu

Abstract

Citation Thurman AR, Doncel GF. Innate immunity and inflammatory response to Trichomonas vaginalis and bacterial vaginosis: relationship to HIV acquisition. Am J Reprod Immunol 2011; 65: 89–98

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.

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