In research published in the Proceedings of the National Academy of Science (PNAS) this week, scientists at Monash University, the Burnet Institute and The Alfred have identified the mechanism of how HIV enters resting cells — the main cell that persists in patients on anti-HIV treatment.
Monash University Professor and Co-Head of the Burnet Institute’s Centre for Virology and Director of The Alfred’s Infectious Diseases Unit, Sharon Lewin said one of the major barriers to curing HIV has been the mystery of how resting cells are infected and how the virus can lie hidden for years in these cells, despite prolonged treatment with anti-HIV drugs.
“Our team of researchers has now identified the path by which the virus can infect resting CD4-T cells and establish latency,” Professor Lewin said.
Latency is the ability of HIV to integrate its genetic material into the genome of resting memory CD4-T-cells where it remains dormant but able to reactivate at some point causing the virus to start replicating.
“We have shown that a family of proteins, called chemokines, that guide resting cells through the blood and into lymph node tissue can ‘unlock the door’ and allow HIV to enter and set up a silent or “latent” infection.
“Once HIV gets into these cells, the virus can then go to sleep. These “silently” infected cells are not cleared by anti-HIV drugs or the immune system. Once a patient stops the anti-HIV drugs, the virus can then wake up and gets going again”.
“Understanding this mechanism will enable new treatment options to be developed which could block latent infection. This new laboratory model of latent HIV infection can also be used to screen drugs that may one day eliminate latent infection,” co-author and Monash clinical immunologist Dr Paul Cameron said.
The research was a collaborative effort involving scientists from the Burnet Institute, The Alfred, Monash University, University of Montreal, Canada and the Westmead Millennium Research Institute in Sydney.
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