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Exploring m6A and m5C Epitranscriptomes upon Viral Infection: an Example with HIV
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Pseudorabies virus exploits N6-methyladenosine modification to promote viral replication
Pei-Lun Yu1,2, Rui Wu1,2, San-Jie Cao1,2
1Department of Preventive Veterinary Medicine, Swine Disease Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.
Frontiers in Microbiology
|February 23, 2023
Summary
N6-methyladenosine (m6A) modification positively regulates pseudorabies virus (PRV) replication and gene expression. This study reveals m6A sites in PRV transcripts, impacting host-virus interactions.
Area of Science:
- Virology
- Molecular Biology
- Epitranscriptomics
Background:
- Pseudorabies virus (PRV), a Herpesviridae family member, causes significant disease in pigs and can infect humans.
- N6-methyladenosine (m6A) is a crucial RNA post-transcriptional modification, but its role in PRV replication is uncharacterized.
Purpose of the Study:
- To investigate the role of m6A modification in the regulation of PRV replication.
- To identify m6A modification sites within PRV transcripts and understand its impact on host-virus interactions.
Main Methods:
- Analysis of m6A abundance in PRV transcripts and its effect on host epitranscriptome.
- Knockdown and overexpression of key m6A regulators (METTL3, METTL14, YTHDF2, YTHDF3, ALKBH5).
- Inhibition of m6A modification using 3-deazaadenosine (3-DAA).
Main Results:
- PRV infection alters the host cell epitranscriptome.
- m6A modification is abundant in PRV transcripts.
- METTL3, METTL14, YTHDF2, and YTHDF3 are essential for PRV replication, while ALKBH5 promotes it.
- Inhibiting m6A modification significantly reduces PRV replication.
Conclusions:
- m6A modification plays a positive regulatory role in PRV replication and gene expression.
- m6A modification dynamically mediates the interaction between PRV and its host.
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