A new study from scientists at the Brigham and Women's Hospital explains how HIV takes advantage of the body, which cellular survival programs become activated and gives a new target for potential therapeutics. The work was published yesterday in Immunity.
"Our work shows that these HIV reservoir cells upregulate anti-apoptosis molecules (molecules that are otherwise expressed in cancer) that maintain their long-term survival," said Mathias Lichterfeld, M.D., Ph.D. "These findings point to clinical strategies that may reduce persisting viral reservoirs."
Using quantitative liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomics, they were able to see what proteins were increased in cells infected with HIV. From that, they were able to find that BIRC5 and OX40 proteins took part in helping HIV reservoir cells survive.
BIRC5 is also known as survivin, which is part of a family of molecules involved in cell death. It's normally expressed in stem cells during embryonic development but turned off in adult cells, except in cancer. In cancer, cells usually turn BIRC5 back on, which helps them stay resistant to chemotherapy. In this work, the researchers believe that BIRC5 may be helping HIV-1 infected cells also escape cell death and possibly help it become resistant to antiretroviral therapy.
The team behind this new study believes that inhibition of the BIRC5-OX40 pathway could reduce the number of HIV reservoir cells and hopefully a new path to eliminate them.