MALAT1 regulates the molecular mechanism of HIV replication.

On February 21st, the international academic journal Nucleic Acid Research published an online research paper by Wang Jianhua of the Shanghai Pasteur Institute of the Chinese Academy of Sciences, "Long noncoding RNA MALAT1 releases epigenetic silencing of HIV-1 by-the-veby by-displacing the polycomb resais 2 from from to the binding the LTR promoter".
the study revealed that long-chain non-coding RNA (LncRNA) MALAT1 induced inhibitory PRC2 (polycomb repress 2) complex dissoced from HIV promoter LTR (long end repetition) and thus promoted HIV transcription and replication.
HIV highly dependent on host factors to complete replication cycles, the identification of key host factors regulating HIV replication can provide a new host target for anti-viral strategy design.
Wang Jianhua's research team used histology techniques to screen a variety of host proteins that can regulate HIV replication, such as host protein SUN2, by maintaining HIV-LTR promoter region heterocolor structure to inhibit HIV transcription and replication (2018, mBio); Phosphinization inhibits its binding with HIV LTR, inhibits hiv transcription, maintains HIV latent (2018, J.Bio.Chem), while host protein Naf1 inhibits HIV replication by inhibiting NF-kB signaling pathways (2016, J. Virol).
in recent years, the important role of long-chain non-coding RNA (LncRNA) in epigenetic regulation, immunomodulation and cell differentiation regulation has attracted wide attention.
can inhibit or promote HIV replication by targeting different cellular protein machines or signaling pathways in regulating HIV infection.
illustration: MALAT1 regulates the molecular mechanism of HIV replication.
MALAT1 induces inhibitory PRC2 complex to dissociate from HIV promoter LTR, and promotes HIV transcription and replication by weakening The H3K27me3 epigenetic modification of EZH2 on the nuclear small body histones in the HIV-LTR region.
LncRNA MALAT1 is highly expressed in tumor cells and is often considered a marker of tumor metastasis.
MALAT1 is mainly located in the nuclear nuclear plaque (Nuclearkle specs) region and can participate in cellular physiological processes such as gene transcription and selective shearing of pre-mRNAs.
Wang Jianhua's team of wuhan university professor Hou Hao used RNA-seq technology to screen out malAT1 in HIV-infected cells high expression; high expression of MALAT1 can promote HIV replication, CRISPR/Cas9 knockout MALAT1 can significantly inhibit HIV-LTR-driven transcription; mechanism, MALAT1 and PRC2 inhibition of the group protein lyinine-methyleenzyme transferEZH2 (enhancer of the Combined to dissociate it from HIV-LTR, weaken editing EZH2 to H3K27me3 epigenetic modification of nuclear small body histones in HIV-LTR region (inhibition), keep HIV-LTR in an active state and promote HIV transcription; Verify the positive correlation between MALAT1 expression and HIV replication.
this study reveals the important role and molecular mechanism of LncRNA MALAT1 regulating HIV replication, and provides a new host target for the design of antiviral strategies.
Qudi and Sun Wei are the first authors of the paper, and Wang Jianhua, Hou Wei and Li Taisheng are side-by-side communication authors.
, Jin Man, a researcher at pasteured Shanghai, made recommendations for the study, which was supported by the National Fund Committee, the Chinese Academy of Sciences and the Ministry of Science and Technology' special prevention and treatment of major infectious diseases of HIV and viral hepatitis.
Source: Pasteur Institute, Shanghai.