N6-methyladenosine (mA) mediates various biological processes by affecting RNA stability, splicing, and translational efficiency. The roles of mA modification in Epstein-Barr virus (EBV) infection in the lytic phase are unclear. Here, knockout of the mA methyltransferase, N6-methyladenosine methyltransferase-like 3 (METTL3), or inhibition of methylation by DAA or UZH1a decreased the expression of viral lytic proteins and reduced progeny virion production. Interestingly, cell growth and viability were decreased by induction of the lytic cycle in METTL3-knockout or inhibitor-treated cells. Apoptosis was induced in those conditions possibly because of a decreased level of the anti-apoptotic viral protein, BHRF1. Therefore, mA shows potential as a target of lytic induction therapy for EBV-associated cancers, including Burkitt lymphoma.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9240777PMC
http://dx.doi.org/10.3389/fmicb.2022.870816DOI Listing

Publication Analysis

Top Keywords

lytic cycle
8
lytic
5
ebv exploits
4
exploits rna
4
rna modification
4
modification promote
4
promote cell
4
cell survival
4
survival progeny
4
progeny virus
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!