Researchers in a new study showed that a drug used to treat certain types of lymphoma was able to dislodge hidden virus in patients receiving treatment for HIV.
Researchers in a new study showed that a drug used to treat certain types of lymphoma was able to dislodge hidden virus in patients receiving treatment for HIV. The researchers are from the University of North Carolina at Chapel Hill found in a new study. The existence of persistent reservoirs of dormant HIV in the immune system that are not attacked by anti-AIDS drugs is believed to be a major reason why infection re-emerges once patients stop taking their medication. The disruption and clearance of these reservoirs is critical to finding a cure for AIDS.
Researchers at UNC, working in collaboration with scientists from the Harvard School of Public Health, National Cancer Institute, Merck, and the University of California at San Diego, undertook a series of experiments designed to evaluate the potential of the drug vorinostat, a deacetylase inhibitor that is used to treat some types of lymphoma, to activate and disrupt the dormant virus.
Initially, laboratory experiments measuring active HIV levels in CD4+ T cells, which are specialized white blood cells that the virus uses to replicate, showed that vorinostat unmasked the hidden virus in these cells. Subsequently, vorinostat was administered to eight HIV-infected men who were medically stable on antiretroviral therapy and the levels of active HIV virus were measured and compared to the levels prior to administration.
Those patients receiving vorinostat showed an average 4.5-fold increase in the levels of HIV RNA in CD4+ T cells, evidence that the virus was being unmasked. This is the first published study to show the potential for deacetylase inhibitors to attack latency within dormant virus pools in a translational clinical study.
"This work provides compelling evidence for a new strategy to directly attack and eradicate latent HIV infection," said David Margolis, MD, professor of medicine, microbiology and immunology, and epidemiology at the University of North Carolina at Chapel Hill.
Targeting latency is the first step on a path that may lead to a cure.
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The study was published in the latest issue of the leading scientific journal, Nature.
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