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

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


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Adolescent
  • Adult
  • Female
  • HIV Infections / immunology
  • HIV Infections / transmission*
  • HIV-1 / pathogenicity*
  • Humans
  • Immunity, Innate
  • Inflammation
  • Middle Aged
  • Risk Factors
  • Trichomonas Vaginitis / epidemiology
  • Trichomonas Vaginitis / immunology*
  • Trichomonas Vaginitis / parasitology
  • Trichomonas vaginalis / pathogenicity*
  • Vaginosis, Bacterial / epidemiology
  • Vaginosis, Bacterial / immunology*
  • Vaginosis, Bacterial / microbiology
  • Young Adult