Is gut dysbiosis a risk factor for HIV infection?

With only a few days to go before World AIDS Day on December 1st, let’s take a look at the links between HIV and the microbiota. Numerous studies have associated changes in the gut microbiome with HIV infection. However, many of these studies have been cross-sectional and methodologically heterogeneous, and therefore subject to various confounding factors. HIV infection is known to be accompanied by gut dysbiosis and bacterial translocation linked to systemic inflammation, but the time course involved is not fully understood. Furthermore, recent studies have shown that, in addition to age, diet, and antibiotic use, sexual behavior also influences the gut microbiota, regardless of HIV status^2,3, further confounding the evidence.

Longitudinal study with bias controlled

 To measure changes in the gut microbiota and markers of inflammation during HIV infection, the researchers selected fecal and blood samples from four different longitudinal studies (USA, Peru) conducted over periods of 4 months to 2 years among men who have sex with men. Of these men, 27 were infected with HIV. The samples from the infected men were paired with those of 28 controls with similar demographic and behavioral characteristics.

Changes in the gut microbiota and inflammatory markers precede seroconversion 

The researchers noted few changes in the gut microbiota of subjects during the acute phase of HIV. In a subgroup from a US study, only an increase in Fusobacterium mortiferum was observed shortly after seroconversion, together with a decrease in Prevotella intermedia. The most significant differences were between pre-HIV infection subjects and controls. The gut microbiota of pre-HIV infection subjects showed reduced levels of several Bacteroides species and a higher level of Megasphaera elsdenii. They also had higher plasma levels of inflammatory cytokines (B cell activating factor, IL-8, TNF-α).

Gut microbiota, a targeted prevention option?

According to the authors, the study suggests that the changes to the gut microbiota existed before HIV infection. Together with similar results from another US team⁴, this shows that gut dysbiosis is a contributing factor to HIV rather than a consequence of it, even if dysbiosis is subsequently observed in chronic HIV. The observation period of the study was too short for the researchers to identify subsequent changes. In addition, the small sample size and the specific characteristics of the participants (sex, age, drug use, sexual behavior, etc.) may also limit generalizability. However, the researchers believe that the discovery of a gut signature for HIV susceptibility and/or inflammatory markers may provide a new tool for targeted prevention.