Herpes simplex virus type 2 (HSV-2)

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.
∗ Corresponding author at: San Antonio Military Medical Center, 3551 Roger
Brooke Drive, Fort Sam Houston, TX 78234, United States. Fax: +1 210 916 5900.
E-mail address: jason.f.okulicz.mil@mail.mil (J.F. Okulicz).
For example, HSV-2 seropositive individuals had a 2-fold greater
risk of HIV acquisition and transmission in prospective studies,
even in those without clinical HSV disease [5,6]. Among
HIV-infected individuals, ongoing high-risk sexual behavior has
important public health implications due to potential transmission
of HIV, HSV, and other sexually transmitted infections (STIs).
HSV co-infection represents a challenge for HIV prevention due
to the high prevalence of genital herpes among HIV-infected populations
worldwide. The most effective method of evaluating HSV
prevalence is by use of serosurveys, since the majority of infections
are subclinical and case reporting underestimates the true burden
of HSV disease [7,8]. HSV-2 seroprevalence among HIV-infected
individuals varies with geographic, social and economic characteristics
with cohort reports ranging from 30 to 70% in the US and
Europe and 50–90% in Africa [7,9–14]. According to National Health
and Nutrition Examination Survey (NHANES) data, HSV seroprevalence
in the US general population has shown a 7% decline in HSV-1