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RNA m6A methylation regulates virus–host interaction and EBNA2 expression during Epstein–Barr virus infection
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RNA m6A methylation regulates virus–host interaction and EBNA2 expression during Epstein–Barr virus infection
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RNA m6A methylation regulates virus–host interaction and EBNA2 expression during Epstein–Barr virus infection
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Journal Article
RNA m6A methylation regulates virus–host interaction and EBNA2 expression during Epstein–Barr virus infection
2021
Overview
Introduction N6‐methyladenosine (m6A) is the most prevalent modification that occurs in messenger RNA (mRNA), affecting mRNA splicing, translation, and stability. This modification is reversible, and its related biological functions are mediated by “writers,” “erasers,” and “readers.” The field of viral epitranscriptomics and the role of m6A modification in virus–host interaction have attracted much attention recently. When Epstein–Barr virus (EBV) infects a human B lymphocyte, it goes through three phases: the pre‐latent phase, latent phase, and lytic phase. Little is known about the viral and cellular m6A epitranscriptomes in EBV infection, especially in the pre‐latent phase during de novo infection. Methods Methylated RNA immunoprecipitation sequencing (MeRIP‐seq) and MeRIP‐RT‐qPCR were used to determine the m6A‐modified transcripts during de novo EBV infection. RIP assay was used to confirm the binding of EBNA2 and m6A readers. Quantitative reverse‐transcription polymerase chain reaction (RT‐qPCR) and Western blot analysis were performed to test the effect of m6A on the host and viral gene expression. Results Here, we provided mechanistic insights by examining the viral and cellular m6A epitranscriptomes during de novo EBV infection, which is in the pre‐latent phase. EBV EBNA2 and BHRF1 were highly m6A‐modified upon EBV infection. Knockdown of METTL3 (a “writer”) decreased EBNA2 expression levels. The emergent m6A modifications induced by EBV infection preferentially distributed in 3ʹ untranslated regions of cellular transcripts, while the lost m6A modifications induced by EBV infection preferentially distributed in coding sequence regions of mRNAs. EBV infection could influence the host cellular m6A epitranscriptome. Conclusions These results reveal the critical role of m6A modification in the process of de novo EBV infection. The viral and cellular N6‐methyladenosine (m6A) epitranscriptomes were changed during de novo Epstein–Barr (EBV) infection in B cells. EBV EBNA2 was a significant m6A‐modified viral transcript, and cellular TLR9 and FAS genes' m6A modification levels are also modulated by EBV infection.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc,Wiley
Subject
