Modifying the antiviral innate immune response by selective writing, erasing, and reading of mA on viral and cellular RNA.

Cell Chem Biol

Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA; Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC 27710, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address:

Published: January 2024

Viral infection and the antiviral innate immune response are regulated by the RNA modification mA. mA directs nearly all aspects of RNA metabolism by recruiting RNA-binding proteins that mediate the fate of mA-containing RNA. mA controls the antiviral innate immune response in diverse ways, including shielding viral RNA from detection by antiviral sensors and influencing the expression of cellular mRNAs encoding antiviral signaling proteins, cytokines, and effector proteins. While mA and the mA machinery are important for the antiviral response, the precise mechanisms that determine how the mA machinery selects specific viral or cellular RNA molecules for modification during infection are not fully understood. In this review, we highlight recent findings that shed light on how viral infection redirects the mA machinery during the antiviral response. A better understanding of mA targeting during viral infection could lead to new immunomodulatory and therapeutic strategies against viral infection.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10872403PMC
http://dx.doi.org/10.1016/j.chembiol.2023.12.004DOI Listing

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