Lentiviral Nef Proteins Differentially Govern the Establishment of Viral Latency

Abstract

Therapeutic attempts to eliminate the latent HIV-1 reservoir have failed, at least in part due to our incomplete biomolecular understanding of how latent HIV-1 infection is established and maintained. We here address the fundamental question of whether all lentiviruses actually possess a similar capacity to establish latent infections or whether there are differences between the lentiviral lineages driving differential latency establishment that could be exploited to develop improved latency reversal agents.

Expression of RNA-m6A-related genes correlates with the HIV latent reservoir level and the CD4+ and CD8+T cell profiles of patients with AIDS

“…However, once the treatment is interrupted, viral replication resumes within a few weeks (6). The reason for this is that HIV DNA integrates into the host cell genome, where it remains in a latent state until conditions are once again favorable for viral replication (20,21). Due to the existence of the HIV latent reservoir, major obstacles to the complete eradication of AIDS remain.…”