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Review
. 2021 Dec 16:12:789605.
doi: 10.3389/fmicb.2021.789605. eCollection 2021.

Regulation of Antiviral Immune Response by N 6-Methyladenosine of mRNA

Baoxin Zhao  1   2 , Weijie Wang  1   2 , Yan Zhao  1   2 , Hongxiu Qiao  1   2 , Zhiyun Gao  1   2 , Xia Chuai  1   2
Affiliations
Free PMC article
Review

Regulation of Antiviral Immune Response by N 6-Methyladenosine of mRNA

Baoxin Zhao et al. Front Microbiol. .
Free PMC article

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, N 6-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.

Keywords: N6-methyladenosine modification; adaptive immunity; immune recognition; innate immunity; viral infection.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Schematic diagram of mechanisms by which m6A modification regulates non-self RNA recognition and innate immune responses. m6A modification in exogenous RNA prevent it from being identified by RNA sensors except for ISG20. Nuclear exportation of MAVS, TRAF3/6, p65, IKKγ, CGAS, and STING mRNA can be accelerated by m6A modification. m6A decoration may be an obstacle to IFNβ and ISGs expression. PTEN, p65 and IKKγ mRNA instability can also be attributed to m6A modification.
FIGURE 2
FIGURE 2
Schematic diagram of mechanisms by which m6A modification regulates adaptive immune responses. m6A modification of SOCS1, SOCS3, CISH mRNA, and lnc-Dpf3 accelerate their decay. Translation of lysosomal cathepsins, including CTSA, CTSB, CTSD, and CTSH, are promoted by m6A and YTHDF1, whereas the expression of ICOS is inhibited by m6A modification.
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