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AIDS. 2018 Mar 27;32(6):687-698. doi: 10.1097/QAD.0000000000001768.

Vaginal microbiota and susceptibility to HIV.

Author information

1
Department of Medicine.
2
Department of Epidemiology.
3
Department of Global Health, University of Washington, Seattle, Washington, USA.

Abstract

: Bacterial vaginosis, characterized by the replacement of the Lactobacillus-dominant microbiota with anaerobic bacteria and facultative Gram-negative rods, has been associated with adverse reproductive health outcomes including HIV acquisition. With the advent of newer molecular techniques, the vaginal microbiota can be investigated in more detail and the association with HIV examined more thoroughly. This review examines recent evidence suggesting that vaginal dysbiosis with increased microbial diversity, specific vaginal bacterial communities, and the presence and concentrations of some individual bacterial species, may increase HIV susceptibility. Potential mechanisms through which vaginal microbiota could impact HIV susceptibility are discussed. On the basis of the available data, this review finds that there is a modest, but growing, body of evidence linking vaginal microbiota to HIV susceptibility in women. The evidence could be strengthened through two main pathways. First, laboratory studies such as ex-vivo or animal experiments are needed to move from plausible mechanisms towards proven mechanisms that explain an effect of the vaginal microbiota on HIV susceptibility. Second, experimental evidence could directly test the hypothesis that sustaining optimal microbiota reduces HIV risk, though there are important obstacles to conducting such studies. Finally, this review examines strong evidence from a recent publication suggesting that deviations from an optimal vaginal microbiome, and particularly the presence of some bacterial communities with high relative abundance of Gardnerella vaginalis, reduces the efficacy of vaginal tenofovir-based microbicides.

PMID:
29424773
PMCID:
PMC5957511
[Available on 2019-03-27]
DOI:
10.1097/QAD.0000000000001768

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