Study links gut-homing protein levels with HIV infection risk, disease progression

For the first time, scientists have shown a relationship between the proportion of key immune cells that display high levels of a gut-homing protein called alpha-4 beta-7 at the time of HIV infection and health outcomes.

Scanning electron micrograph of a human T lymphocyte (also called a T cell) from the immune system of a healthy donor. Image credit: NIAID

The new study found that women who had more CD4+ T cells displaying high levels of alpha-4 beta-7 on their surface were more likely to become infected with HIV, and the virus damaged their immune systems more rapidly, than women with fewer such cells.

The research team compared the percentage of CD4+ T cells displaying high levels of alpha-4 beta-7 in blood samples drawn from 59 women shortly before they acquired HIV to the percentage of such cells in 106 women who remained HIV negative.

The proportion of CD4+ T cells with high levels of alpha-4 beta-7 had an effect, albeit modest, on the risk of acquiring HIV. The risk of HIV acquisition rose by 18 percent for each one percent increase in alpha-4 beta-7 protein.

The proportion of CD4+ T cells with high levels of alpha-4 beta-7 strongly affected how quickly HIV damaged the immune system. CD4+ T cell levels declined twice as fast among women with higher pre-infection levels of alpha-4 beta-7 as among women with lower pre-infection levels.

In addition, the amount of HIV in the blood within a few months of infection was greater in women with higher pre-infection levels of alpha-4 beta-7 than in women with lower pre-infection levels.

The mechanism for the immune system damage likely was HIV-related damage to the gut, the scientists report, as higher pre-infection levels of alpha-4 beta-7 were associated with higher levels of a biological marker of gut damage.

The scientists found that HIV targets CD4+ T cells displaying alpha-4 beta-7 very early in infection, particularly in the gut.

Starting antiretroviral therapy (ART) right after HIV diagnosis did not prevent the depletion of CD4+ T cells from the gut or facilitate reconstitution of the depleted cells.

These findings suggest that interventions in addition to ART may be needed to restore CD4+ T cells in the GI tracts of people living with HIV. One such intervention could be an anti-alpha-4 beta-7 antibody called vedolizumab, which is FDA-approved for the treatment of ulcerative colitis and Crohn’s disease. (National Institutes of Health)

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