Proposed mechanisms by which T. vaginalis infection may increase HIV-1 infection include inducing the inflammatory response of vaginal, exocervix, and urethral epithelia; disrupting mucosal barrier function; recruitment of CD4 lymphocytes and macrophages; development of microhemorrhages; degrading secretory leukocyte protease inhibitors; and enhancing susceptibility to bacterial vaginosis or other abnormal vaginal flora that may increase the risk of HIV-1 acquisition [161–164]. This evidence concerns the gene CD4 and HIV-1 infection.