Modifying the antiviral innate immune response by selective writing, erasing, and reading of m6A on viral and cellular RNA

被引:6
|
作者
Aufgebauer, Caroline J. [1 ]
Bland, Katherine M. [1 ]
Horner, Stacy M. [1 ,2 ,3 ]
机构
[1] Duke Univ, Sch Med, Dept Mol Genet & Microbiol, Durham, NC 27710 USA
[2] Duke Univ, Sch Med, Dept Integrat Immunobiol, Durham, NC 27710 USA
[3] Duke Univ, Sch Med, Dept Med, Durham, NC 27710 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
RIG-I; NUCLEOTIDE-SEQUENCES; DISCRIMINATING SELF; BINDING-PROTEIN; STRANDED-RNA; NUCLEAR-RNA; N-6-METHYLADENOSINE; METHYLATION; RECOGNITION; REVEALS;
D O I
10.1016/j.chembiol.2023.12.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Viral infection and the antiviral innate immune response are regulated by the RNA modification m6A. m6A directs nearly all aspects of RNA metabolism by recruiting RNA -binding proteins that mediate the fate of m6A-containing RNA. m6A 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 m6A and the m6A machinery are important for the antiviral response, the precise mechanisms that determine how the m6A 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 m6A machinery during the antiviral response. A better understanding of m6A targeting during viral infection could lead to new immunomodulatory and therapeutic strategies against viral infection.
引用
收藏
页码:100 / 109
页数:10
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