Epigenetic Modifications in Viral Infections, Volume II

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: closed (1 July 2025) | Viewed by 598

Special Issue Editors


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Guest Editor
Department of Microbiology and Immunology, University of Otago, Dunedin 9054, New Zealand
Interests: molecular virology; influenza virus; viral pathogenesis; virus–host interactions; innate antiviral response; post-translational protein modifications; protein trafficking; acetylation; HDACs; HATs
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Guest Editor
Institute of Environmental Science and Research, Wallaceville, Upper Hutt 5018, New Zealand
Interests: molecular virology; proteomics; bioinformatics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epigenetic modifications, e.g., methylation and acetylation of host DNA, RNA, and proteins such as histones play a critical role in host biology during viral infection. Similarly, these epigenetic modifications also occur in viral DNA, RNA, and proteins and influence the inter- and intramolecular interactions between viral and host components. Viruses tend to exploit these modifications in their favor to facilitate their infection and pathogenesis. New findings in this area continue to unravel with the invention and application of new genomic and proteomic research technologies. A detailed understanding of the role of epigenetic modifications in viral infection is key to elucidate the mechanisms of virus–host interactions and viral pathogenesis and design targeted antiviral strategies. This Special Issue of Viruses invites articles reporting on the latest research developments in this exciting area of virology research.

Dr. Matloob Husain
Dr. Farjana Ahmed
Guest Editors

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Keywords

  • viral pathogenesis
  • virus–host interaction
  • epigenetic modifications
  • acetylation
  • methylation
  • proteomics
  • genomics

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Published Papers (1 paper)

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Research

18 pages, 2943 KiB  
Article
IFI16 Mediates Deacetylation of KSHV Chromatin via Interaction with NuRD and Sin3A Co-Repressor Complexes
by Anandita Ghosh, Bala Chandran and Arunava Roy
Viruses 2025, 17(7), 921; https://doi.org/10.3390/v17070921 - 28 Jun 2025
Viewed by 202
Abstract
IFI16 is a well-characterized nuclear innate immune DNA sensor that detects foreign dsDNA, including herpesviral genomes, to activate the inflammasome and interferon pathways. Beyond immune signaling, IFI16 also functions as an antiviral restriction factor, promoting the silencing of invading viral genes through transcriptional [...] Read more.
IFI16 is a well-characterized nuclear innate immune DNA sensor that detects foreign dsDNA, including herpesviral genomes, to activate the inflammasome and interferon pathways. Beyond immune signaling, IFI16 also functions as an antiviral restriction factor, promoting the silencing of invading viral genes through transcriptional and epigenetic mechanisms. We recently demonstrated another role of IFI16, in which it interacts with and recruits the class I histone deacetylases, HDAC1 and 2, to the KSHV latency protein LANA, modulating its acetylation and function. In this study, we asked whether these IFI16-HDAC1/2 interactions contribute to broader epigenetic regulation of the KSHV chromatin. Our findings reveal that IFI16 associates with and facilitates the recruitment of the NuRD and Sin3A co-repressor complexes—both multiprotein, HDAC1/2-containing chromatin regulators—on KSHV episomes. Depletion of IFI16 led to reductions in NuRD and Sin3A occupancy on viral chromatin, accompanied by increased histone acetylation at lytic gene promoters. These results suggest that IFI16 plays a critical role in recruiting or stabilizing these HDAC-containing co-repressor complexes on the KSHV genome, thereby enforcing transcriptional silencing of lytic genes and maintaining latency in KSHV. Our study expands the known functions of IFI16 and identifies a novel epigenetic mechanism by which it modulates herpesviral chromatin states. Full article
(This article belongs to the Special Issue Epigenetic Modifications in Viral Infections, Volume II)
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