Abstract
Bacterial vaginosis (BV) is a disorder of the female reproductive tract (FRT) in which a healthy Lactobacillus-dominant microflora is replaced by BV-associated bacteria. In the clinic, BV can significantly increase the incidence of HIV acquisition in women; however, to date mechanistic evidence has been scant. In this issue, Cherne and colleagues (e00041-20) demonstrate that BV disrupts the FRT by triggering the expression of host-derived enzymes, which increase HIV infection. Their studies also suggest that matrix metalloproteinase inhibition in the FRT could be a novel target to limit or prevent HIV transmission.
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