While the design of this study cannot determine the exact mechanisms by which T. vaginalis might mediate an increased risk of HIV infection in ESN, the failure of T. vaginalis infection to increase percent expression of activated T cell phenotypes CD38 and HLADR suggests that T cell activation along the CD38 and HLADR pathways may not be the predominant mode by which T. vaginalis could facilitate endocervical HIV transmission. Here, CD38 is linked to HIV infectious disease.