Regulation of Antiviral Immune Response by N6-Methyladenosine of mRNA

Abstract

Host innate and adaptive immune responses play a vital role in clearing infected viruses. Meanwhile, viruses also evolve a series of mechanisms to weaken the host immune responses and evade immune defense. Recently, N6-methyladenosine (m6A), the most prevalent mRNA modification, has been revealed to regulate multiple steps of RNA metabolism, such as mRNA splicing, localization, stabilization, and translation, thus participating in many biological phenomena, including viral infection. In the process of virus–host interaction, the m6A modification that presents on the virus RNA impedes capture by the pattern recognition receptors, and the m6A modification appearing on the host immune-related molecules regulate interferon response, immune cell differentiation, inflammatory cytokine production, and other immune responses induced by viral infection. This review summarizes the research advances about the regulatory role of m6A modification in the innate and adaptive immune responses during viral infections.

N6-methyladenosine (m6A) writer METTL3 accelerates the apoptosis of vascular endothelial cells in high glucose

“…M 6 A modification has been proposed to be participated in cardiovascular physiological and pathological processes [ [18] , [19] , [20] ]. However, the vital roles of m 6 A writer METTL3 in high glucose exposure vascular endothelial cells are unknown [ 21 , 22 ].…”

Identification and Characterization of BmNPV m6A Sites and Their Possible Roles During Viral Infection

“…Increasing data showed that YTHDF readers regulate the mRNA fate of cellular or viral m6A RNAs. It is described to regulate splicing, nuclear export, cap-independent translation, and decay ( 46 ). To better understand the regulatory effects of m6A machinery on the expression of viral genes or viral replication, the expression level of IE-1 was detected from BmN cells transfected with the wild-type and mutant ie-1 plasmids, and Western blotting assay exhibited a higher IE-1 expression level on the mutant plasmid than wild-type ie-1 , confirming that the presence of m6A sites in the ie-1 mRNA may be related to its expression.…”

Impact of N6-methyladenosine (m6A) modification on immunity

“…Studies demonstrate that m 6 A modification tightly controls various innate immune responses such as the expression of interferons (IFNs), inflammatory responses, and macrophages and dendritic cells homeostasis. m 6 A can either improve the immune response against pathogens and viruses or tame the immune response to prevent aggressive immunopathological damage [46]. 6 A of these transcripts enhanced their translation in DCs via YTHDF1, thus promoting DCs activation and stimulating DC-mediated T cell activation [49].…”