Trichomonas vaginalis adhesion protein 33 (TvAP33) promotes HPV infection by upregulating the expression of HPV membrane receptor molecules.

Abstract

An increasing number of studies have identified Trichomonas vaginalis (T. vaginalis) as a risk factor for human papillomavirus (HPV) infection, yet experimental data and the mechanisms involved are still lacking. Wild-type and T. vaginalis adhesion protein 33 (TvAP33) knockdown T. vaginalis were used to infect HaCaT cells and the vaginal tissue of mice, while HaCaT cells were also transfected to overexpress TvAP33. The effects of TvAP33 on the expression of HPV membrane receptor molecules and HPV infection were assessed. Infection of HaCaT cells with low expression of HPV membrane receptor molecules by T. vaginalis with reduced TvAP33 expression was conducted to analyze whether TvAP33 influences HPV infection through HPV membrane receptor molecules. In this study, we found that T. vaginalis significantly enhances HPV invasion into HaCaT cells and the mouse vagina while also increases the expression of HPV receptor molecules CD151 and HSPG2. Reducing the expression of TvAP33 led to a significant decrease in both HPV invasion rate and CD151/HSPG2 expression. Conversely, overexpressing TvAP33 in HaCaT cells resulted in a notable increase in HPV invasion and CD151/HSPG2 expression. Additionally, the simultaneous reduction of TvAP33 expression in T. vaginalis and CD151/HSPG2 expression in HaCaT cells further decreased HPV invasion rates. These findings suggest that TvAP33 promotes HPV infection by upregulating CD151 and HSPG2 expression. This study not only confirms, through both in vivo and in vitro experiments, that T. vaginalis facilitates HPV infection but also explores the mechanism by which TvAP33 enhances HPV infection by regulating HPV receptor expression. These results provide a theoretical basis for understanding the mechanisms of T. vaginalis co-infection with HPV.