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A new study by investigators at Brigham and Women’s Hospital explores how the virus gets this foothold, identifying cellular survival programs that become activated in infected cells, and providing a potential target for future therapy. HIV reservoir cells upregulate anti-apoptosis molecules (molecules that are otherwise expressed in cancer) that maintain their long-term survival,” said Mathias Lichterfeld, MD, Ph.D., of BWH’s Division for Infectious Diseases.
BIRC5 and OX40 were both involved in these cells’ long-term survival. BIRC5, also known as “survivin” is part of a family of molecules involved in cell death. It is naturally expressed in stem cells during embryonic development but generally turned off in adult cells. One exception to this generality is cancer: cancer cells frequently turn BIRC5 back on and its presence is associated with resistance to chemotherapy.
The new study shows BIRC5 may help HIV-1- infected cells to escape cell death, and contribute to the ability of viral reservoir cells to persist for decades despite effective antiretroviral therapy. Patients with HIV who have had aggressive chemotherapy that has temporarily reduced viral levels to undetectable levels, but HIV has rebounded in the patients. Inhibition of the BIRC5-OX40 pathway may reduce reservoirs of infected cells, and potentially offer a path forward to eliminating these persisting cells.
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