Figure 4.

m⁶A modification is involved in antiviral responses of innate immunity. (A) DDX46, which forms a complex with ALKBH5, inhibits antiviral responses by reducing m⁶A modification-mediated nucleus export and translation of MAVS, TRAF3, and TRAF6 transcripts. (B) hnRNPA2B1 enhances antiviral responses by preventing FTO-mediated demethylation on STING, CGAS, and IFI16 transcripts. (C) During VSV infection, the enzymatic activity of ALKBH5 is decreased, which results in increasing m⁶A level. The upregulation of m⁶A modification leads to decreasing the expression of OGDH transcripts and reprograming host cell metabolism, which consequently enhancing antiviral responses. (D) m⁶A modification suppresses antiviral responses by repressing the production and stability of IFNB mRNA stability. VSV, vesicular stomatitis virus; TRAF3, TNF receptor-associated factor 3; TRAF6, TNF receptor-associated factor 6; HSV-1, herpes simplex virus-1; STING, stimulator of interferon response CGAMP interactor 1; CGAS, cyclic GMP-AMP synthase; IFI16, interferon gamma inducible protein 16; OGDH, α-ketoglutarate dehydrogenase; HCMV, Human cytomegalovirus; dsDNA, double stranded DNA; IFNB, IFN-beta.