Katherine M Bruner1, Lillian B Cohn2. 1. Department of Molecular Biosciences, The University of Texas at Austin, Texas. 2. Chan Zuckerberg Biohub, San Francisco, California, USA.
Abstract
PURPOSE OF REVIEW: To provide a summary of the recent data examining infected CD4+ T cell dynamics during ART and implications for cure strategies. RECENT FINDINGS: HIV-1 cure is a worldwide unmet medical need. Although combination antiretroviral therapies effectively suppress HIV-1 replication in vivo, viral rebound occurs shortly after therapy cessation. The major barrier to HIV-1 cure is a pool of latently infected CD4+ T cells, called the latent reservoir, which is established early during infection, has a long half-life in vivo, and is not eliminated by treatment. It was thought that the stability of the reservoir came from long-lived latently infected CD4+ T cells, but more recent data suggests that the reservoir is dynamic, such that there is an equilibrium in which proliferation of HIV-1-infected cells is offset by an equivalent loss of cells harboring HIV-1 DNA. SUMMARY: We review the evidence to support this dynamic model of persistence, mechanisms by which infected cells expand and are eliminated, and discuss the impact of a dynamic reservoir on the future of HIV-1 cure studies.
PURPOSE OF REVIEW: To provide a summary of the recent data examining infectedCD4+ T cell dynamics during ART and implications for cure strategies. RECENT FINDINGS:HIV-1 cure is a worldwide unmet medical need. Although combination antiretroviral therapies effectively suppress HIV-1 replication in vivo, viral rebound occurs shortly after therapy cessation. The major barrier to HIV-1 cure is a pool of latently infectedCD4+ T cells, called the latent reservoir, which is established early during infection, has a long half-life in vivo, and is not eliminated by treatment. It was thought that the stability of the reservoir came from long-lived latently infectedCD4+ T cells, but more recent data suggests that the reservoir is dynamic, such that there is an equilibrium in which proliferation of HIV-1-infected cells is offset by an equivalent loss of cells harboring HIV-1 DNA. SUMMARY: We review the evidence to support this dynamic model of persistence, mechanisms by which infected cells expand and are eliminated, and discuss the impact of a dynamic reservoir on the future of HIV-1 cure studies.
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