Innate immunity and inflammatory response to Trichomonas vaginalis and bacterial vaginosis: relationship to HIV acquisition.
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.
Thurman
Andrea R
AR
Department of Obstetrics and Gynecology, CONRAD Clinical Research Center and CONRAD Microbicide Research Laboratory, Eastern Virginia Medical School, Norfolk, VA 23507, USA. thurmaar@evms.edu
Doncel
Gustavo F
GF
D000293:Adolescent; D000328:Adult; D005260:Female; D015658:HIV Infections / Q000276:immunology / Q000635:transmission*; D015497:HIV-1 / Q000472:pathogenicity*; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation; D008875:Middle Aged; D012307:Risk Factors; D014247:Trichomonas Vaginitis / Q000453:epidemiology / Q000276:immunology* / Q000469:parasitology; D014246:Trichomonas vaginalis / Q000472:pathogenicity*; D016585:Vaginosis, Bacterial / Q000453:epidemiology / Q000276:immunology* / Q000382:microbiology; D055815:Young Adult