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Updated: May 30, 2025

Exploring m6A and m5C Epitranscriptomes upon Viral Infection: an Example with HIV
Published on: March 5, 2022
The role of N6-methyladenosine (m6A) mRNA modifications in herpesvirus infections
Ruth Verhamme1, Herman W Favoreel1
1Department of Translational Physiology, Infectiology and Public Health, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
Abstract:
Herpesviruses, a family of large enveloped DNA viruses, establish persistent infections in a wide range of hosts. This characteristic requires an intricate network of interactions with their hosts and host cells. In recent years, the interplay between herpesviruses and the epitranscriptome-chemical modifications in transcripts that may affect mRNA biology and fate-has emerged as a novel aspect of herpesvirus-host interactions. In particular, herpesviruses display different mechanisms to modulate and usurp the most abundant mRNA modification, N6-methyladenosine or m6A. Some herpesviruses interfere with m6A methylation of transcripts, while others enhance or take advantage of m6A methylation of viral and/or cellular transcripts. In many cases, herpesviruses appear to modulate the m6A methylation process to suppress the antiviral host response. This review highlights the strategies used by members of the different herpesvirus subfamilies to manipulate host m6A mediators and how these contribute to virus replication and the antiviral host response. Research aimed at deciphering the interaction of herpesviruses with the m6A epitranscriptome not only may lead to new avenues in the design of antiviral and immunomodulatory strategies, but also provides new insights in the regulation and the role of m6A transcript methylation in general.
Insights
Herpesviruses manipulate N6-methyladenosine (m6A) RNA modifications to establish persistent infections. Understanding these interactions can lead to new antiviral strategies and insights into m6A regulation.
Area of Science:
- Virology
- Molecular Biology
- Epitranscriptomics
Background:
- Herpesviruses are large DNA viruses known for establishing persistent infections.
- These viruses engage in complex interactions with host cells.
- The epitranscriptome, particularly N6-methyladenosine (m6A) modifications, is a new frontier in understanding virus-host dynamics.
Purpose of the Study:
- To review the diverse strategies herpesviruses employ to modulate host m6A epitranscriptome.
- To elucidate how these manipulations impact viral replication and host antiviral responses.
- To highlight the potential for therapeutic interventions based on these interactions.
Main Methods:
- Literature review of studies on herpesvirus-m6A interactions.
- Analysis of mechanisms by which herpesviruses alter m6A methylation.
- Synthesis of findings on the role of m6A in viral persistence and host immune evasion.
Main Results:
- Herpesviruses utilize distinct strategies to interfere with, enhance, or exploit m6A methylation of viral and cellular transcripts.
- Modulation of m6A is frequently observed to suppress antiviral host responses.
- These viral strategies are conserved across different herpesvirus subfamilies.
Conclusions:
- Herpesviruses actively manipulate the host m6A epitranscriptome for their own benefit.
- Targeting these virus-host epitranscriptomic interactions offers promising avenues for antiviral drug development.
- Further research into m6A regulation by viruses will deepen our understanding of both viral pathogenesis and fundamental RNA biology.
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