A truncated HIV Tat demonstrates potent and specific latency reversal activity

E Van Gulck, Marion Pardons, Erik Nijs, Nick Verheyen, Koen Dockx, Christel van den Eynde, Emilie Battivelli, Jerel Vega, E Florence, Brigitte Autran, Nancie M. Archin, David M. Margolis, Christine Katlama, Chiraz Hamimi, Ilse Van den Wyngaert, Filmon Eyassu, Linos Vandekerckhove, Daniel Boden

    Research output: Contribution to journalA1: Web of Science-articlepeer-review


    A major barrier to HIV-1 cure is caused by the pool of latently infected CD4 T-cells that persist under combination antiretroviral therapy (cART). This latent reservoir is capable of producing replication-competent infectious viruses once prolonged suppressive cART is withdrawn. Inducing the reactivation of HIV-1 gene expression in T-cells harboring a latent provirus in people living with HIV-1 under cART may result in depletion of this latent reservoir due to cytopathic effects or immune clearance. Studies have investigated molecules that reactivate HIV-1 gene expression, but to date, no latency reversal agent has been identified to eliminate latently infected cells harboring replication-competent HIV in cART-treated individuals. Stochastic fluctuations in HIV-1 tat gene expression have been described and hypothesized to allow the progression into proviral latency. We hypothesized that exposing latently infected CD4+ T-cells to Tat would result in effective latency reversal. Our results indicate the capacity of a truncated Tat protein and mRNA to reactivate HIV-1 in latently infected T-cells ex vivo to a similar degree as the protein kinase C agonist: phorbol 12-myristate 13-acetate, without T-cell activation or any significant transcriptome perturbation.
    Original languageEnglish
    Article numbere0041723
    JournalAntimicrobial Agents and Chemotherapy
    Issue number11
    Number of pages22
    Publication statusPublished - 2023


    • HIV
    • Tat
    • Latency


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