Trichomonas vaginalis-induced epithelial monolayer disruption and human immunodeficiency virus type 1 (HIV-1) replication: implications for the sexual transmission of HIV-1.
The objective of this study was to evaluate potential mechanisms of Trichomonas vaginalis involvement in human immunodeficiency virus type 1 (HIV-1) transmission. Polarized monolayer integrity of primary cervical and prostate epithelial cells or cell lines cultured with T. vaginalis was measured by monitoring transepithelium resistance. The effect of T. vaginalis isolates on HIV-1 passage through polarized epithelial cell monolayers was evaluated for HIV-1 p24gag in the basolateral supernatants. Coincubation with T. vaginalis isolates induced disruption of monolayer integrity and resulted in passage of virus to the basolateral side of the monolayer. Furthermore, there was isolate variability in which two isolates induced greater monolayer damage and increased HIV-1 passage than did the other two isolates. Coincubation of T. vaginalis isolates with acutely HIV-1-infected peripheral blood mononuclear cells enhanced HIV-1 replication. This enhancement was associated with cellular proliferation and activation, as well as with tumor necrosis factor alpha production. In contrast to the monolayer disruption, the effect of T. vaginalis on HIV-1 replication was not isolate dependent. Thus, two mechanisms have been identified that could contribute to the epidemiologic association of trichomoniasis with the sexual transmission of HIV-1. (i) T. vaginalis disruption of urogenital epithelial monolayers could facilitate passage of HIV-1 to underlying layers. (ii) Activation of local immune cells by T. vaginalis in the presence of infectious HIV-1 might lead to increased viral replication. Collectively, these data suggest the need for more vigilant efforts in the diagnosis and treatment of T. vaginalis in women and men, especially in countries with a high prevalence of HIV-1.
Guenthner
Patricia C
PC
HIV and Retrovirology Branch, Division of HIV/AIDS Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Mail Stop G19, Atlanta, Georgia 30333, USA.
Secor
W Evan
WE
Dezzutti
Charlene S
CS
D000163:Acquired Immunodeficiency Syndrome / Q000635:transmission*; D000818:Animals; D002460:Cell Line; D002584:Cervix Uteri / Q000276:immunology* / Q000821:virology; D004847:Epithelial Cells / Q000276:immunology* / Q000502:physiology / Q000821:virology; D005260:Female; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D008297:Male; D011467:Prostate / Q000276:immunology* / Q000821:virology; D012749:Sexually Transmitted Diseases / Q000635:transmission*; D014246:Trichomonas vaginalis / Q000472:pathogenicity*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D014779:Virus Replication
D014409:Tumor Necrosis Factor-alpha