Genital epithelial cells (ECs) are the first line of defense that sexually transmitted viruses encounter. Quite a high possibility, is it not? The prevalence of detection of HHV8 was 32% in saliva samples, 28% in mouth swabs, 4% in cervical swabs, 2.3% in vaginal swabs, 9% in plasma samples, and 18% in PBMC samples. “Most HSV-2 infections are acquired from persons without a clinical history of genital herpes,” they note. There were no significant differences in HSV shedding among the subgroups of women starting combination oral contraceptives containing both estrogen and progesterone or progesterone-only contraceptives. The reduction was greater in participants with a history of genital herpes (74%) than in those without such a history (30%). Essential information was collected using a questionnaire.
11.2%). HIV infection was associated with iDC depletion in the cervix, and with increased HSV2 genital reactivation, which in turn was associated with HIV shedding levels. Taken together, our observations indicate a low prevalence of HSV DNA genital shedding in adult Senegalese women. We hypothesize that frequent HSV-2 genital shedding causes increased levels of inflammatory cytokines, such as IL-1 and IFN-?, and decreased levels of antiviral innate immune molecules (i.e. secretory leukocyte protease inhibitor, SLPI) and that these changes result in fluctuations in the vaginal microbiome which predispose women to develop BV. The mucosal surface in the genital tract is the primary route of infection of most sexually transmitted infections; more than 70% of human immunodeficiency virus (HIV)-1 transmission occurs across the genital epithelium . If a person has both herpes simplex virus 1 and 2, having virus 1 does not determine how often the person will shed type 2 virus.
In a survey of 736 participants in this cohort, we found the seroprevalence of HHV8 to be 44% . “The issue of infectivity is both a patient management and a public health concern. Relationships between HSV-2 shedding and Nugent score, quantity and presence of BVAB, and cytokine levels will be determined. These women will then be placed on suppressive acyclovir, which decreases HSV-2 shedding by 70-80%. We will determine whether suppression of HSV-2 shedding results in improved vaginal flora as measured by a decrease in Nugent score and increased concentration of lactobacilli. However, a study among HSV-2 discordant couples found that over an 8-month period, the incidence of HSV-2 seroconversion was only 3.6% 10. Ultimately, this proposal will contribute vital and novel information to the design of interventions that can modulate BV, and will provide us with knowledge to better promote women’s reproductive health.
Herpes simplex virus type 2 (HSV-2) and bacterial vaginosis (BV) are two of the most common infections of the female genital tract;both are associated with an increased risk for acquiring HIV infection, and they are associated with each other. The goal of this research is to understand the relationship between HSV-2 and BV in women, using daily genital sampling to determine whether HSV-2 shedding increases the risk of colonization with vaginal bacteria associated with BV, through modulating inflammatory markers in the genital tract. This research will lead to improved understanding of the impact of HSV-2 on vaginal bacteria and inflammation, and will provide insight into the interventions needed to better promote women’s reproductive health.