AI Article Synopsis
- Pseudorabies virus (PRV) is a disease-causing virus primarily affecting pigs, with emerging evidence of human infections, and its relationship with RNA modifications is being explored.
- The study found that mA modification was prominent in PRV transcripts and that manipulating certain host proteins significantly influenced PRV replication; inhibiting or enhancing these proteins affected the virus's ability to replicate.
- Overall, the research suggests that mA modification plays a crucial role in facilitating PRV replication and gene expression, highlighting its dynamic interaction with host cells.
Article Abstract
Introduction: Pseudorabies virus (PRV) is the pathogenic virus of porcine pseudorabies (PR), belonging to the family. PRV has a wide range of hosts and in recent years has also been reported to infect humans. N-methyladenosine (mA) modification is the major pathway of RNA post-transcriptional modification. Whether mA modification participates in the regulation of PRV replication is unknown.
Methods: Here, we investigated that the mA modification was abundant in the PRV transcripts and PRV infection affected the epitranscriptome of host cells. Knockdown of cellular mA methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of mA modification by 3-deazaadenosine (3-DAA), a mA modification inhibitor, could significantly reduce viral replication.
Results And Discussion: Taken together, mA modification played a positive role in the regulation of PRV replication and gene expression. Our research revealed mA modification sites in PRV transcripts and determined that mA modification dynamically mediated the interaction between PRV and host.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9936159 | PMC |
| http://dx.doi.org/10.3389/fmicb.2023.1087484 | DOI Listing |
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