HIV susceptibility in women: The roles of genital inflammation, sexually transmitted infections and the genital microbiome.

Given that heterosexual transmission of HIV across the genital mucosa is the most common route of infection in women, an in-depth understanding of the biological mechanisms associated with HIV risk in the female genital tract (FGT) is essential for effective control of the epidemic. Genital pro-inflammatory cytokines are well-described biological co-factors to HIV risk. Increased levels of pro-inflammatory cytokines in the FGT have been associated with a 3-fold higher-risk of acquiring HIV, presumably through involvement in barrier compromise and the recruitment of highly activated HIV target cells to the site of initial viral infection and replication. Sexually transmitted infections (STIs) and bacterial vaginosis (BV) are suggested possible contributors to genital inflammation in the FGT, and this, coupled with the relationship between genital inflammation and HIV risk, underscores the importance of effective treatment of STI and BV in the promotion of women's health. In most low- and middle-income countries, STIs are treated syndromically, a practice providing rapid treatment without identifying the infection source. However, this approach has been associated with over-diagnosis and the overuse of drugs. Further, because many women with STIs are asymptomatic, syndromic management also fails to treat a vast proportion of infected women. Although several studies have explored the role of STIs and the vaginal microbiome on genital inflammation and HIV risk, the impact of STI and BV management on genital inflammation remains poorly understood. This review aimed to collate the evidence on how BV and STI management efforts affect genital inflammation and the genital microbiome in women.