Defective HIV proviruses reprogram immune cells to promote viral persistence

Researchers at the Leibniz Institute of Virology report that defective HIV proviruses are not inert leftovers of infection. When these genetic remnants integrate into the BACH2 gene, they reprogram CD4 T-like cells, pushing them toward long-term survival and continued division and altering their immune state. This mechanism may help explain how the virus persists in the body despite suppressive treatment, since infected cells carrying the defective proviruses are not eliminated but instead sustained. The findings point to provirus integration site and host-gene effects as a factor in the reservoir that current therapies do not address. How broadly this pathway operates across patients, and whether it can be targeted therapeutically, are open questions.

Written by a model from the reports · updated 4 hours ago