Evaluation of Health Disparity in Bacterial Vaginosis and the Implications for HIV-1 Acquisition in African American Women

Abstract

There is a health disparity for both bacterial vaginosis (BV) and human immunodeficiency virus type 1 (HIV-1) infection in African American women that may be linked. The evidence that BV predisposes women to higher risk for HIV infection is well documented. The underlying mechanisms to support the epidemiological connections will require further investigations. This review explores the risk factors for BV disease with implications for HIV-1 acquisition in the context of race as a potential driver of the 20-fold increase in HIV-1 acquisition for African American women compared to white women. Specifically, it explores (i) disparities for BV in African American women, (ii) racial disparity for HIV-1 acquisition in African American women, (iii) common factors associated with BV and HIV acquisition in African American women, and (iv) potential mechanisms of the enhancement of HIV-1 transmission by BV.

Keywords: BV; inflammation; pathogenesis; race; stress; vaginal epithelium.

Figure 1

Exposure of vaginal epithelial cells to Gardnerella vaginalis results in upregulation of proinflammatory cytokines, namely IL‐6, IL‐8, TNF‐α, and IL‐1β. Vimentin is upregulated after G. vaginalis exposure. Upregulation of vimentin influences uptake and internalization of bacteria. Tight junction proteins (TJ) ZO1 and ZO2 are downregulated in vaginal epithelial cells exposed to G. vaginalis. Downregulation of TJ proteins could result in HIV passing in between cells (paracellular transport) in route to the vaginal submucosa where subepithelial T cells and macrophages reside and are highly permissive for HIV infection. Trafficking of infected T cells by resident lymph nodes would facilitate HIV dissemination via the blood.