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    Area of Science:

    • Virology
    • Molecular Biology
    • Immunology

    Background:

    • Human Immunodeficiency Virus type 1 (HIV-1) establishes latent reservoirs in host cells, primarily CD4+ T cells and microglia, hindering complete eradication.
    • Host factors maintaining viral latency are crucial for viral persistence but remain incompletely understood, posing challenges for therapeutic interventions.

    Purpose of the Study:

    • To identify host factors that stabilize key transcriptional regulators involved in maintaining HIV-1 latency.
    • To investigate the role of the ENL-USP7 complex in suppressing HIV-1 transcription and sustaining viral quiescence.
    • To explore the therapeutic potential of targeting the ENL-USP7-BRD4 axis for HIV-1 latency reversal.

    Main Methods:

    • Identification and characterization of the ENL-USP7 protein complex.
    • Biochemical assays to determine the interaction between USP7, BRD4, and ENL.
    • Utilizing Proteolysis-Targeting Chimeras (PROTACs) to disrupt the ENL-USP7 complex.
    • Assessing HIV-1 reactivation in cellular models, primary CD4+ T cells, and microglia from individuals on antiretroviral therapy.

    Main Results:

    • The YEATS domain-containing protein ENL and its associated deubiquitinase USP7 form a complex that maintains HIV-1 latency.
    • USP7 stabilizes BRD4 through deubiquitination, which suppresses HIV-1 transcription and promotes viral quiescence.
    • Disruption of the ENL-USP7 complex using PROTACs successfully reactivated latent HIV-1 in cell lines, primary CD4+ T cells, and microglia.
    • The ENL-USP7-BRD4 axis was identified as a critical mechanism enforcing HIV-1 latency.

    Conclusions:

    • The ENL-USP7-BRD4 axis is a key regulator of HIV-1 latency, stabilizing viral transcriptional machinery.
    • Targeting USP7 or ENL presents a promising therapeutic vulnerability for reactivating latent HIV-1 reservoirs.
    • USP7 inhibition or disruption of the ENL-USP7 complex offers a potential strategy for latency-reversing therapies in HIV-1 treatment.