December 19 2016
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Research from the UNC School of Medicine published in the Journal of Clinical Investigation shows that a new antibody might be the answer.
A team led by Dr. Lishan Su proved that by interfering with the signaling of persistent type 1 interferon, a cellular protein, it limits a pathway linked to immune activation, thus promoting immune recovery as well as viral suppression when used in with combination with antiretrovirals.
Su’s team used humanized mouse models of HIV infection, and injected them with a unique antibody. As a result, they saw the mice had reversed immune hyper-activation, which led to a reduction in T-cell exhaustion, a reversal of HIV-specific T-cell function, thus suppressing viral loads much faster and easier.
“cART stops the growth of the virus but cannot achieve HIV-1 eradication,” Dr. Liang Cheng, the first author of the paper and a research associate in Su’s lab, noted in a statement. “The virus rebounds quickly when cART is discontinued because there are reservoirs of HIV-1 that persist during cART; therapy does not work against these reservoirs. The recovered adaptive immune response to HIV can help to eliminate the HIV-1 reservoirs and control the virus rebound after cART discontinuation.”
Even for patients who are virally suppressed, chronic immune activations can be a major problem. Thanks to Su’s team, we now know it’s possible to deactivate the immune response, giving the immune system — which is already fighting against the virus — a chance to recuperate and regenerate much needed T-cells.
“This technique may be of help to those patients whose viral replication is suppressed but who are unable to fully recover immunologically,” Su said. “It may help to control or reduce HIV-1 reservoirs in all cART-treated patients. And this could potentially help cure HIV infection.”
Read more articles from PLUS, here.
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