Abstract

Antiretroviral Therapy (ART) can suppress Human Immunodeficiency Virus (HIV) replication almost completely, to the extent that plasma viremia is undetectable by standard clinical tests. Yet this intervention is not curative, as ART withdraw usually results in viremic rebound to pre-ART levels within several weeks. The HIV reservoir, comprised primarily of persistent CD4⁺ T cells harboring replication-competent proviruses integrated into host cell genomes, is the primary the source of viremic rebound upon ART withdrawal and principal barrier to a cure. Reservoir persistence is enabled by two principal characteristics: T cell clonal expansion and proviral transcriptional suppression, or latency. In a recent authoritative review, select genetic, epigenetic, cellular, and immunological determinants of these reservoir characteristics, interdependencies among these determinants, and implications for HIV-1 persistence were presented and discussed.

Keywords: Human Immunodeficiency Virus (HIV); Persistence; Transcriptional regulation; T cell; Clonal expansion; HIV rebound