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    Home > Biochemistry News > Biotechnology News > Fudan University mBio published a paper: Discovering new key genes for latent HIV infection

    Fudan University mBio published a paper: Discovering new key genes for latent HIV infection

    • Last Update: 2021-10-11
    • Source: Internet
    • Author: User
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    Zhu Huanzhang team AIDS is an infectious disease caused by human immunodeficiency virus (HIV) infection that seriously endangers people's lives and health
    .
    At present, the clinical treatment of AIDS is mainly antiretroviral therapy.
    Although this therapy can inhibit the virus replication in the patient to the greatest extent, reduce the plasma viral load to a level that cannot be detected by the existing conventional testing methods.
    However, once it is stopped With drug treatment, the viral load will rebound to the pre-treatment level

    .
    An important reason why AIDS cannot be cured is due to the long-term existence of a latent virus reservoir composed of HIV latent infected cells, and the molecular mechanism of how HIV-1 latent cells are formed and maintained has not yet been elucidated

    .


    Recently, the team of Professor Zhu Huanzhang of Fudan University published an online publication titled "FKBP3 induces human immunodeficiency virus-1 latency by recruiting histone deacetylase 1/2 to the viral long terminal repeat" (FKBP3 induces human immunodeficiency virus-1 latency by recruiting histone deacetylase 1/2 to the viral long terminal repeat" on the internationally renowned magazine mbio.
    Enzyme 1/2 to the LTR region of the virus induces HIV-1 latent).
    The newly identified important HIV-1 latent gene FKBP3 (or FKBP25) has been reported internationally, revealing that FKBP3 is involved in HIV through epigenetic modification.
    It plays a key role in the establishment and maintenance of latency, and it has been confirmed that in the early stage of HIV-1 infection, T lymphocytes promote FKBP3 expression through interferon-gamma to inhibit HIV-1 infection

    .
    This study provides a new understanding of the mechanism of HIV latent infection and replication, and provides a potential drug intervention target for the functional treatment of AIDS

    .

    In this work, the researchers verified the potential candidate gene FKBP3 that is potentially related to HIV-1 on the basis of the large-scale CRISPR-Cas9 gene knockout screening, and found that multiple HIV-1 latently infected cell lines Knockout of FKBP3 in the latent model of CD4+ T lymphocytes and primary CD4+ T lymphocytes can promote latent HIV-1 transcriptional activation; at the same time, studies have found that FKBP3 can interact with YY1, HDAC1 and HDAC2 proteins, and can indirectly bind to HIV-1 through YY1 LTR region, and recruit HDAC1 and HDAC2 to HIV-1 LTR region, causing the level of histone acetylation near the HIV-1 integration site to decrease, leading to HIV-1 latent; the researchers also found that when HIV-1 infects cells The human body’s inherent innate immunity can increase the expression level of FKBP3 by secreting IFN-gamma, thereby inhibiting HIV-1 infection and replication, and inducing HIV-1 latency
    .


    In recent years, Zhu Huanzhang’s team has focused on the molecular mechanism of HIV latency and discovered that histone methyltransferases GLP, miRNA (miR-196b and miR-1290) and PEBP1 play an important role in the maintenance of HIV latency (EMBO).
    Reports, 2020, 21 (11): e49305; Virology, 2013, 440, 182-189; Virology, 2015; 486: 228-38)

    .


    Professor Zhu Huanzhang’s team Dr.
    Yang Xinyi is the first author of the paper, and Professor Zhu Huanzhang is the corresponding author

    .
    Relevant research has been funded by the National Infectious Disease Major Special Project, the National Natural Science Foundation of China NSFC-NIH Cooperation Project and the National Natural Science Foundation of China General Project

    .

    The full text link is as follows: https://journals.
    asm.
    org/doi/10.
    1128/mBio.
    00795-21

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