T-Cell Marker May Lead to Improved Treatment for HIV

Researchers at George Mason University have found a measurable indicator that may prove beneficial in restoring T cell mobility within patients with HIV. The study, which was recently published in the Science Advance, focused on cofilin, a key protein that regulates cells mobility and the ability to fight against infection.

Cofilin dysfunction is a key factor in helper T cell defects in a patient with HIV. Helper T cells are vital to the immune system for their ability to recognize a foreign antigen and help form an immunized response.

"When you have an infection, you need to mobilize the T cells," said Yuntao Wu, PhD, co-author of the study. "In HIV infection, there is a profound depletion of helper T cells in lymphoid tissues, such as those in the gut."

According to Wu, HIV naturally leads to multiple immune defects, such as T cell migration impairment. Furthermore, although antiretroviral therapy (ART) has significantly increased the lifespan of HIV-infected people, it is not a cure or a means for full immune system restoration, according to the researchers.

The study found that those with HIV have "significantly lower" levels of cofilin phosphorylation. Phosphate serves as a regulator for cofilin activity and is needed for cells to move in and out of tissues. Since ART cannot restore the level of cofilin phosphorylation, the research team concluded that it could not be a stand-alone cure.

By stimulating the T cells with additional therapeutics, such as the alpha 4 beta 7 integrin antibody, researchers could modulate the levels of cofilin activity needed to restore T cell mobility. According to the press release, the remedy has shown lasting effects in immune control of simian immunodeficiency virus (SIV), the simian form of the AIDS virus, in a monkey trial; however, it did not show the same results in HIV-infected human patients.

"Now we have a marker, and at least one target that we can focus on to discover new therapies to repair the immune damages for a functional cure," Wu said.

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