Herpes simplex virus type 2 (HSV-2) plays an important role
in the dynamics of human immunodeficiency virus (HIV) infection.
HSV-2 enhances HIV acquisition through genital ulceration,
which provides a portal of entry for HIV, and upregulates activated
immune cells associated with HSV-2 infection, which may
increase the number of immune targets for HIV infection [1]. Subclinical
genital erosions in the setting of HSV-2 infection are also
thought to facilitate HIV transmission by promoting HIV shedding
in the genital tract [2–4]. Studies have demonstrated the
clinical significance of HSV in the epidemiology of HIV infection.