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Researchers at University of California, San Diego School of Medicine have discovered that HIV infection of human immune cells triggers a massive increase in methylation, a chemical modification, to both human and viral RNA, aiding replication of the virus. The study, published February 22, 2016 in Nature Microbiology, identifies a new mechanism for controlling HIV replication and its interaction with the host immune system. “We and other colleagues at pharmaceutical companies have worked over the years to develop drugs targeting HIV’s genetic material, its RNA, but we never made it to the clinic,” said senior author Tariq Rana, PhD, professor of pediatrics at UC San Diego School of Medicine. “Now we know why — we were developing drugs using RNA targets that didn’t have these modifications, when in reality the RNA was different.” In the study, Rana’s team discovered m6A modifications in HIV RNA for the first time. They also examined m6A’s effect on function in both HIV and human host RNA during infection of human immune cells. “M6A had always been considered a steady modification of cellular RNA. Instead, it turned out to be extremely dynamic and highly responsive to external stimuli, such as viral infections” said Gianluigi Lichinchi, a graduate student in Rana’s lab and first author of the study. “In the future, these findings could aid in improving the design and efficacy of HIV/AIDS vaccines.” Read more Funding: This research was funded, in part, by the National Institutes of Health (grants EB020393, NS076465, AI43198, DA039562, DA030199), Sloan Foundation, Bert L. and N. Kuggie Vallee Foundation, Irma T. Hirschl and Monique Weill-Caulier Charitable Trusts, WorldQuant Foundation and STARR Consortium. Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community.
