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Updated: Sep 27, 2025

Exploring m6A and m5C Epitranscriptomes upon Viral Infection: an Example with HIV
Published on: March 5, 2022
Pathogenic Roles of m6A Modification in Viral Infection and Virus-driven Carcinogenesis
Jia-Feng Wang1, Wei Cai2, Fen-Sheng Qiu1
1Zhejiang Provincial Laboratory of Experimental Animal's & Nonclinical Laboratory Studies, Hangzhou Medical College, Hangzhou, China.
Abstract:
N6-methyladenosine (m6A) is a prevalent modification of RNA in eukaryotes, bacteria, and viruses. It is highly conserved and can affect the structure, localization, and biology functions of RNA. In recent years, multiple m6A methylation sites have been identified in the viral RNA genome and transcripts of DNA viruses. This modification occurs commonly during the primary infection and is dynamically regulated by a methyltransferase (writers), demethylase (eraser) and m6A-binding proteins (readers) within the host cells. The abnormal m6A modification not only affects the replication of pathogenic viruses and host immune response but also contributes to the pathogenesis of virus-induced cancers. In this review, we highlight recent advances on the mechanism of m6A modification on viral replication, host immune response and carcinogenesis to provide a novel insight for epigenetic prevention of viral infection and virus-driven carcinogenesis.
Insights
N6-methyladenosine (m6A) RNA modification impacts viral replication and host immunity. Understanding m6A
Area of Science:
- Molecular Biology
- Epigenetics
- Virology
Background:
- N6-methyladenosine (m6A) is a widespread RNA modification in various organisms, influencing RNA's structure, localization, and function.
- m6A sites are found in viral RNA genomes and DNA virus transcripts, playing a role during primary infection.
- This modification is dynamically regulated by writers, erasers, and readers within host cells.
Purpose of the Study:
- To review recent advances in understanding m6A modification in viral replication.
- To explore the role of m6A in host immune response during viral infections.
- To highlight m6A's contribution to virus-induced carcinogenesis and potential epigenetic prevention strategies.
Main Methods:
- Literature review of recent studies on m6A modification in viral contexts.
- Analysis of mechanisms linking m6A to viral replication, host immunity, and cancer development.
- Synthesis of findings to provide insights into epigenetic strategies.
Main Results:
- m6A modification is dynamically regulated during viral infection by host cellular machinery.
- Aberrant m6A patterns affect pathogenic viral replication and modulate host immune responses.
- m6A dysregulation is implicated in the pathogenesis of virus-associated cancers.
Conclusions:
- m6A modification is a critical epigenetic regulator in virus-host interactions.
- Targeting m6A pathways offers potential for novel antiviral therapies and cancer prevention.
- Further research into m6A mechanisms can illuminate new avenues for epigenetic interventions.
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