Review
Version 1
Preserved in Portico This version is not peer-reviewed
HIV Expression in Infected T Cell Clones
Version 1
: Received: 14 December 2023 / Approved: 14 December 2023 / Online: 14 December 2023 (16:51:16 CET)
A peer-reviewed article of this Preprint also exists.
Rausch, J.W.; Parvez, S.; Pathak, S.; Capoferri, A.A.; Kearney, M.F. HIV Expression in Infected T Cell Clones. Viruses 2024, 16, 108. Rausch, J.W.; Parvez, S.; Pathak, S.; Capoferri, A.A.; Kearney, M.F. HIV Expression in Infected T Cell Clones. Viruses 2024, 16, 108.
Abstract
The principal barrier to an HIV-1 cure is the persistence of infected cells harboring replication-competent proviruses despite antiretroviral therapy (ART). HIV-1 transcriptional suppression, referred to as viral latency, is foremost among persistence determinants, as it allows infected cells to evade the cytopathic effects of virion production and killing by cytotoxic T lymphocytes (CTL) and other immune factors. HIV-1 persistence is also governed by cellular proliferation, an innate and essential capacity of CD4+ T cells that both sustains cell populations over time and enables a robust directed response to immunological threats. Yet when HIV-1 infects CD4+ T cells, this capacity for proliferation can counterproductively enable surreptitious HIV-1 propagation without the deleterious effects of viral gene expression in latently infected cells. Over time on ART, the HIV1 reservoir is shaped by both persistence determinants, with selective forces most often favoring clonally expanded infected cell populations harboring transcriptionally quiescent proviruses. Moreover, if HIV latency is incomplete or sporadically reversed in clonal infected cell populations that are replenished faster than they are depleted, such populations could both persist indefinitely and contribute to low-level persistent viremia during ART and viremic rebound if treatment is withdrawn. In this review, select genetic, epigenetic, cellular, and immunological determinants of viral transcriptional suppression and clonal expansion of HIV-1 reservoir T cells, interdependencies among these determinants, and implications for HIV-1 persistence will be presented and discussed.
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Keywords
human immunodeficiency virus (HIV); persistence; transcriptional regulation; T cell; clonal expansion; HIV rebound
Subject
Biology and Life Sciences, Virology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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