The Microbiome and Risk for HIV

Research in South Africa shows how the balance of bacteria in a woman’s vagina can raise or lower her risk for HIV

December 6, 2016

Mailman School Epidemiology Professor Salim Abdool Karim had a question: why were young women in Africa at higher risk of acquiring HIV infection than young men? Studies conducted by the Mailman School–affiliated Centre for the AIDS Program of Research in South Africa (CAPRISA) showed that women aged 15 to 24 in that country are upward of four times more likely to be infected with HIV than their male counterparts.

Analyzing data from a clinical trial of a vaginal microbicide, Karim, director of CAPRISA, and his immunology team found that vaginal inflammation accurately predicted which women would get infected with HIV. The finding raised another important question: what was behind the inflammation that was putting women at risk for HIV?

To learn more, Karim called Ian Lipkin, director of the Center for Infection and Immunity (CII). “The question we wanted to address was whether differences in the populations of bacteria, fungi, or other microbes might be driving the inflammation,” says Lipkin. “Implicating microbes in inflammation and HIV risk had the potential to lead to new methods for preventing infection.”

Brent Williams, an assistant professor of Epidemiology with expertise in microbiome research, led the effort, which continued even without outside funding. He examined the genetic profiles of vaginal microorganisms sampled from 119 women. Women who had the bacterium Prevotella bivia in their vaginas were 19 times more likely to have vaginal inflammation and almost 13 times more likely to contract HIV. On the other hand, some bacteria appeared to have a protective effect: women with Megasphaera and BVAB-1 were 10 times less likely to acquire the disease.

Exactly how microbes affect risk for HIV is still unclear but factors may include damage to the vaginal mucosa, recruitment of cells susceptible to infection, or inhibiting the growth of “good bacteria” that protect against invasion.

In ongoing research, Williams aims to zero in on other suspect bacteria potentially involved in vaginal inflammation and HIV transmission. “The more we understand about the bacteria that are increasing or decreasing the risk for HIV,” he says, “the greater our capacity to target those bacteria or modulate the immune system in order to reduce HIV acquisition.”

Managing bacteria to reduce vaginal inflammation could be a cost-effective way to curb the spread of HIV in low-income countries hardest hit by the epidemic. In southern and eastern Africa alone, an estimated 380,000 young women aged 16-24 are infected each year.

“Reducing new HIV infections in young women is one of the greatest challenges in southern Africa,” said Karim. “Based on our results, implementing a combination of evidence-based targeted interventions to break the cycle of HIV transmission while effectively treating bacterial vaginosis could enhance HIV prevention in women in the highest HIV-burden region of the world.”