RNA anti-cyclone enzyme DDX46 can significantly inhibit interferon expression induced by viral infection.

On August 29th, the journal Nature-Immunology published a paper by Cao Xuetao, president of the Chinese Academy of Medical Sciences and a member of the Chinese Academy of Engineering, reporting on the results of the study that RNA derotorase DDX46 can cause antiviral effect molecule mRNA nucleus retention through RNA demethylation modification, thereby inhibiting the natural immune response of antivirals.
interferon plays a key role in the body's natural antiviral immune response.
in the process of virus infection, the amount and duration of interferon production is precisely regulated to ensure that the body clears the invading virus while avoiding pathological autoimmune damage.
current research on the molecular mechanism of precise regulation of interferon expression is mainly focused on natural immune signaling pathogen molecules, while the mechanism of regulating interferon expression in the way of RNA modification in the nucleus is not clear.
Cao Xuetao, a postdoctoral fellow at the Institute of Basics of the Chinese Academy of Medical Sciences, and Hou Jin, a professor at the National Key Laboratory of Medical Immunology at the Second Military Medical University, jointly attacked the role of members of the DEAD-box derivease (DDX) family in RNA identification and metabolism and their important function in regulating antiviral natural immune response, and found that DDX46 can significantly suppress the expression of viral infection by screening the role of members of the DDX family in the natural immune response of virally infected macrophages.
studies have shown that DDX46 binds to the CCGGUU conservative base sequence of antiviral effect molecule mRNA, and the binding of DDX46 to m6A demethylase ALKBH5 increases when the virus is infected. The de-methylation modification of antiviral effect molecule mRNA in combination with DDX46 causes its nuclear retention, which blocks the protein expression of these antiviral effect molecules and reduces interferon production, which ultimately inhibits the natural immune response of antiviral.
This study reveals that RNA anti-cytase DDX46 participates in the regulation of antiviral natural immune response through a new way of RNA modification in the nucleus, and proposes a new natural immune and inflammatory regulatory mechanism, which provides new potential targets and ideas for the prevention and treatment of viral infections and inflammatory diseases.
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