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

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.