Researchers at the University of California, Davis, have identified a target for therapeutic intervention and agents that disrupt HIV latency in patients under suppressive HIV therapy. It amplifies the effects of other latency reversal agents and primes the cells harboring the virus for immune clearance and death.
Immune cells harboring latent HIV in patients who are under suppressive antiretroviral therapy (ART) cannot be detected by the host’s immune system. Although transcriptional activation of latent HIV has been reported in some current medical research, the potency is low, creating a barrier to eliminating HIV.
Researchers at the University of California, Davis, have discovered a novel epigenetic modification that regulates HIV transcription. Induction of the target through chemical agents disrupts HIV latency and activates HIV replication within HIV latency cell line models in vitro and resting CD4+ T cells isolated from patients under ART ex vivo. In addition, this treatment amplifies other effects of latency reversal agents, such as Histone Deacetylase inhibitors or Protein Kinase C agonists, and may prime the immune cells harboring any latent HIV for immune clearance and death. These findings have identified a novel epigenetic target for flushing out latent HIV.
HIV, HIV latency, HIV cure, immune cells, suppressive antiretroviral therapy, suppressive therapy, antireotroviral, HIV reactivation, latency reversal, HIV replication, ART