A study1 has looked into the mechanism of the inflammatory response induced by bacterial vaginosis (BV) in the vagina and cervix. 

There are typically quite a variety of inflammatory markers found in women with BV when swabs are taken, with some of these inflammatory markers are proposed to increase the risk of HIV-1 acquisition. Interestingly, BV doesn’t cause the obvious signs of inflammation, like redness, swelling or pain. At the mucosal level, inflammation is more obvious in terms of markers produced. This inflammation results in some negative clinical outcomes, including almost double the chance of contracting HIV and three times the risk of transmitting HIV to a male partner.

Why is genital mucosal inflammation a cause of increased HIV acquisition? Possibly because the mucosal integrity is disrupted, the protection of innate immunity is altered, and there are an increase in the number of HIV target cells on the mucosal surface. Early after HIV is deposited into the vagina is the uptake of the virus by CD4 T cells, or via the Langerhans cells, located inside the epithelium of the vagina and/or cervix, which then transfers the virus to the CD4 T cells. Transmission may also occur in the upper reproductive tract.

It isn’t known how, why and when BV causes vaginal mucosa inflammation.

Key findings of the study

  • Women who acquired HIV were found (prior to seroconversion – that is, a positive HIV test can be made due to sufficient antibodies being produced by the body) to have higher levels of beta-defensin 2, an antimicrobial peptide, in vaginal secretions and more Escherichia coli bactericidal activity than non-seroconverters
  • Seronegative sex workers over multiple studies have been shown to have lower levels of inflammatory cytokines in vaginal secretions compared to those in HIV-positive and HIV-negative controls
  • HIV acquisition in those on hormonal contraceptives showed higher levels of RANTES and lower levels of secretory leukocyte protease inhibitor in women who acquired HIV (previous studies)
  • Suggested findings are that higher levels of vaginal inflammation and lower levels of anti-inflammatory factors are associated with higher levels of HIV virus transmission across the vaginal mucosa
  • Some BV-related species have greater pro-inflammatory potential than others
  • Cocultures developed with Atopobium vaginae, Mobiluncus curtisii, Prevotella bivia or G. vaginalis induce much higher levels of inflammatory markers than Lactobacillus species
  • Other study results demonstrate that BV-associated bacterial species can induce an innate immune response from vaginal epithelial tissue by upregulation of cytokines that are associated with an increased risk of HIV-1 transmission
  • Stimulatory potential between species occurs
  • It is not completely understood, but there is evidence regarding the role of Lactobacillus species in reducing inflammatory markers in the vagina
  • Genetic testing has revealed that some women respond differently to Gram-negative rods

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  1.  Bacterial Vaginosis and the Cervicovaginal Immune Response, Mitchell C, Marrazzo J, American Journal of Reproductive Immunology-6-71 (2014)

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