It has been over 10 years since reports were published that sexually transmitted infections (STIs) facilitate the transmission of HIV infection, and 8 years since the first review of the subject. None of these early reports mentioned bacterial vaginosis (BV). Following initial in vitro work by Klebanoff and Coombs in 1991, which suggested that BV may facilitate HIV transmission,¹ it was not until the clinical observations of Cohen et al in 1995² that the association between BV and HIV transmission has become a focus of attention (although other work was probably ongoing). There may be two broad reasons for the delay in recognition of the association.

Firstly, there is conflicting opinion as to whether BV is an STI. For this reason, researchers concentrating on the link between STIs and HIV infection may have simply “overlooked” the disease. Secondly, limited knowledge of the microenvironment and pathological response of the vagina affected by BV probably led researchers away from considering whether BV might affect HIV transmission. The enhancing effect of STIs on HIV transmission has generally focused on broken mucosal/skin defences, inflammatory exudates, or bleeding as reasons why STIs increase transmission of HIV. BV is not characterised by these vaginal changes.

An understanding is emerging of how BV might enhance the susceptibility to HIV infection.³ The vagina is normally colonised by Lactobacillus species. Lactobacilli produce lactic acid, which maintains a low vaginal pH and inhibits the growth of many micro-organisms, including those associated with BV. Additionally, some lactobacilli—particularly those that “protect” against development of BV—produce hydrogen peroxide, which is toxic to a number of micro-organisms, including HIV.¹ BV is characterised by an absence of lactobacilli and, thus, an elevated pH. A low vaginal pH may inhibit CD4 lymphocyte activation and therefore decrease HIV target cells in the vagina …