REVIEW article
Front. Pharmacol.
Sec. Inflammation Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1667283
This article is part of the Research TopicDeep Learning-Assisted Discovery and Evaluation of Novel Anti-RNA Virus Drugs Targeting m6A ModificationView all articles
Role of N6-Methyladenosine (m6A) Epitranscriptomic Mark in Regulating Viral Infections and Target for Antiviral Development
Provisionally accepted
- 1Texas Biomedical Research Institute, San Antonio, United States
- 2Lancaster University, Lancaster, United Kingdom
- 3Virology, Lancaster University, Lancaster, United Kingdom
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Viral infectious diseases continue to pose significant public health threats, driving severe epidemics and occasional pandemics of great consequences to humans. Viral infections trigger a range of transcriptional and epitranscriptional changes, including N6-methyladenosine (m6A) modification—one of the most abundant and dynamic RNA methylation marks. Although m6A mark was identified decades ago, its functional relevance in viral RNA remained elusive until recent advances in sequencing technologies. Viruses, like their host cells, depend on mRNA for protein synthesis and must rapidly replicate and evade host immune responses. This review focuses on the critical role of m6A in the regulation of viral infections and immune responses. Herein, we explore the most recent advances on how viruses exploit the m6A marks and host m6A machinery to enhance their replication and how host m6A modifications can influence viral pathogenicity. Understanding the interplay between m6A modifications and viral life cycles will be important for the potential of targeting m6A regulatory proteins as novel antiviral strategies to control viral infections. Moreover, a better understanding of these mechanisms will contribute to deeper insights into the host innate immune response and the development of innovative antiviral therapeutics.
Keywords: antiviral, drug, M6A, RNA, Therapeutics, viral infection
Received: 16 Jul 2025; Accepted: 01 Sep 2025.
Copyright: © 2025 Bayoumi, Manju, Martinez-Sobrido and Munir. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Muhammad Munir, Virology, Lancaster University, Lancaster, 75189, United Kingdom
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