HIV transmission is modulated by the vaginal microbiota. Women colonised with optimal vaginal bacterial communities, typically dominated by a beneficial Lactobacillus spp., have a decreased risk of acquiring and transmitting HIV compared to women colonised with ‘non-optimal’ microbiota (e.g. bacterial vaginosis, BV) that promote subclinical genital inflammation driving increased HIV risk. BV is characterised by depletion of Lactobacillus spp. and a high relative abundance or load of facultative and/or obligate anaerobes.1 While studies have focused on the association between vaginal microbiome (including specific taxa), and HIV risk, relatively little is known about the role of metabolites produced by vaginal microbiota and their role in modifying the cervicovaginal environment including interaction with epithelial cells that form a physical and immunological barrier in the female reproductive tract. Major distinguishing features between women colonised with an optimal (L. crispatus dominated) versus non-optimal vaginal microbiota (i.e. BV) include lower vaginal pH (pH<4.5 vs pH>4.5) and dramatically increased vaginal levels of lactic acid (~120 mM vs <20 mM) suggesting that lactic acid is an effector molecule produced by beneficial Lactobacillus spp. that may play a role in modulating HIV acquisition.2 This presentation will review our current knowledge of the multifaceted activity of lactic acid including its antimicrobial and direct immune modulatory3,4,5 and epithelial barrier enhancing properties on cervicovaginal epithelial cells. How this bioactive could potentially be used to optimise the vaginal environment and microbiome to help prevent HIV will be discussed.
1McKinnon LR et al 2019. AIDS Res Hum Retroviruses 35:219
2Tachedjian G et al 2017 Res Microbiol 168:782
3Hearps AC et al 2017 Mucosal Immunol 10:1480
4Delgado-Diaz DJ et al 2020 Front Cell Infect Microbiol 9:446
5Tyssen D et al 2018 mSphere 3:e00055-18