Abstract
N6-methyladenosine (m6A) is a ubiquitous RNA modification in eukaryotes. It plays important roles in the translocation, stabilization and translation of mRNA. Many recent studies have shown that the dysregulation of m6A modification is connected with diseases caused by pathogenic viruses, and studies on the role of m6A in virus-host interactions have shown that m6A plays a wide range of regulatory roles in the life cycle of viruses. Respiratory viruses are common pathogens that can impose a large disease burden on young children and elderly people. Here, we review the effects of m6A modification on respiratory virus replication and life cycle and host immunity against viruses.
Highlights
RNA posttranscriptional modification is very common in eukaryotes, and more than one hundred types of modifications have been reported to date (Boccaletto et al, 2018)
According to the research of Price, the early and late viral transcripts of adenovirus include methyltransferase-like 3 (METTL3)-dependent m6A modifications, but m6A is not necessary for the early phase of adenovirus infection (Price et al, 2020). This group knocked out METTL3 or METTL14 and infected cells 48 h later, and the early gene replication and transcription products of the virus were found to be basically unaffected after infection, but the production of late RNA, late protein, and infectious progeny was significantly reduced in the METTL3- and METTL14knockout cells (Price et al, 2020)
We discussed the latest developments in the role of m6A methylation in the life cycle of respiratory viruses
Summary
RNA posttranscriptional modification is very common in eukaryotes, and more than one hundred types of modifications have been reported to date (Boccaletto et al, 2018). The role of the m6A modification in the replication of respiratory viruses and its effect on the host immune response are discussed. Price et al (2020) found that after adenovirus infection of A549 cells, the expression levels of other interacting enzymes did not change significantly, except for a slight increase in the levels of FTO and ALKBH5, and the host proteins were concentrated at the sites of early viral RNA synthesis.
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