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Viruses
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Epigenetic Modifications in Viral Infections
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Epigenetic Modifications in Viral Infections

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 11856

Special Issue Editors

Dr. Matloob Husain

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals
Dr. Farjana Ahmed

E-Mail Website
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 on 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 the latest research developments in this exciting area of virology research.

Dr. Matloob Husain
Dr. Farjana Ahmed
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (5 papers)

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Research

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27 pages, 28803 KiB  
Article
Epigenetic Modifications of White Blood Cell DNA Caused by Transient Fetal Infection with Bovine Viral Diarrhea Virus
by Hana Van Campen, Jeanette V. Bishop, Zella Brink, Terry E. Engle, Carolina L. Gonzalez-Berrios, Hanah M. Georges, Jessica N. Kincade, Dilyara A. Murtazina and Thomas R. Hansen
Viruses 2024, 16(5), 721; https://doi.org/10.3390/v16050721 - 1 May 2024
Viewed by 1732
Abstract
Bovine viral diarrhea virus (BVDV) infections cause USD 1.5–2 billion in losses annually. Maternal BVDV after 150 days of gestation causes transient fetal infection (TI) in which the fetal immune response clears the virus. The impact of fetal TI BVDV infections on postnatal [...] Read more.
Bovine viral diarrhea virus (BVDV) infections cause USD 1.5–2 billion in losses annually. Maternal BVDV after 150 days of gestation causes transient fetal infection (TI) in which the fetal immune response clears the virus. The impact of fetal TI BVDV infections on postnatal growth and white blood cell (WBC) methylome as an index of epigenetic modifications was examined by inoculating pregnant heifers with noncytopathic type 2 BVDV or media (sham-inoculated controls) on Day 175 of gestation to generate TI (n = 11) and control heifer calves (n = 12). Fetal infection in TI calves was confirmed by virus-neutralizing antibody titers at birth and control calves were seronegative. Both control and TI calves were negative for BVDV RNA in WBCs by RT-PCR. The mean weight of the TI calves was less than that of the controls (p < 0.05). DNA methyl seq analysis of WBC DNA demonstrated 2349 differentially methylated cytosines (p ≤ 0.05) including 1277 hypomethylated cytosines, 1072 hypermethylated cytosines, 84 differentially methylated regions based on CpGs in promoters, and 89 DMRs in islands of TI WBC DNA compared to controls. Fetal BVDV infection during late gestation resulted in epigenomic modifications predicted to affect fetal development and immune pathways, suggesting potential consequences for postnatal growth and health of TI cattle. Full article
(This article belongs to the Special Issue Epigenetic Modifications in Viral Infections)
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Review

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18 pages, 790 KiB  
Review
Epigenetic Control of Innate Immunity: Consequences of Acute Respiratory Virus Infection
by Rivka Bella Lefkowitz, Clare M. Miller, Juan David Martinez-Caballero and Irene Ramos
Viruses 2024, 16(2), 197; https://doi.org/10.3390/v16020197 - 27 Jan 2024
Cited by 3 | Viewed by 2681
Abstract
Infections caused by acute respiratory viruses induce a systemic innate immune response, which can be measured by the increased levels of expression of inflammatory genes in immune cells. There is growing evidence that these acute viral infections, alongside transient transcriptomic responses, induce epigenetic [...] Read more.
Infections caused by acute respiratory viruses induce a systemic innate immune response, which can be measured by the increased levels of expression of inflammatory genes in immune cells. There is growing evidence that these acute viral infections, alongside transient transcriptomic responses, induce epigenetic remodeling as part of the immune response, such as DNA methylation and histone modifications, which might persist after the infection is cleared. In this article, we first review the primary mechanisms of epigenetic remodeling in the context of innate immunity and inflammation, which are crucial for the regulation of the immune response to viral infections. Next, we delve into the existing knowledge concerning the impact of respiratory virus infections on the epigenome, focusing on Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), Influenza A Virus (IAV), and Respiratory Syncytial Virus (RSV). Finally, we offer perspectives on the potential consequences of virus-induced epigenetic remodeling and open questions in the field that are currently under investigation. Full article
(This article belongs to the Special Issue Epigenetic Modifications in Viral Infections)
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23 pages, 1119 KiB  
Review
Epigenetic Restriction Factors (eRFs) in Virus Infection
by Arunava Roy and Anandita Ghosh
Viruses 2024, 16(2), 183; https://doi.org/10.3390/v16020183 - 25 Jan 2024
Viewed by 2278
Abstract
The ongoing arms race between viruses and their hosts is constantly evolving. One of the ways in which cells defend themselves against invading viruses is by using restriction factors (RFs), which are cell-intrinsic antiviral mechanisms that block viral replication and transcription. Recent research [...] Read more.
The ongoing arms race between viruses and their hosts is constantly evolving. One of the ways in which cells defend themselves against invading viruses is by using restriction factors (RFs), which are cell-intrinsic antiviral mechanisms that block viral replication and transcription. Recent research has identified a specific group of RFs that belong to the cellular epigenetic machinery and are able to restrict the gene expression of certain viruses. These RFs can be referred to as epigenetic restriction factors or eRFs. In this review, eRFs have been classified into two categories. The first category includes eRFs that target viral chromatin. So far, the identified eRFs in this category include the PML-NBs, the KRAB/KAP1 complex, IFI16, and the HUSH complex. The second category includes eRFs that target viral RNA or, more specifically, the viral epitranscriptome. These epitranscriptomic eRFs have been further classified into two types: those that edit RNA bases—adenosine deaminase acting on RNA (ADAR) and pseudouridine synthases (PUS), and those that covalently modify viral RNA—the N6-methyladenosine (m6A) writers, readers, and erasers. We delve into the molecular machinery of eRFs, their role in limiting various viruses, and the mechanisms by which viruses have evolved to counteract them. We also examine the crosstalk between different eRFs, including the common effectors that connect them. Finally, we explore the potential for new discoveries in the realm of epigenetic networks that restrict viral gene expression, as well as the future research directions in this area. Full article
(This article belongs to the Special Issue Epigenetic Modifications in Viral Infections)
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16 pages, 766 KiB  
Review
Functional Impacts of Epitranscriptomic m6A Modification on HIV-1 Infection
by Stacia Phillips, Tarun Mishra, Siyu Huang and Li Wu
Viruses 2024, 16(1), 127; https://doi.org/10.3390/v16010127 - 16 Jan 2024
Cited by 6 | Viewed by 2102
Abstract
Epitranscriptomic RNA modifications play a crucial role in the posttranscriptional regulation of gene expression. N6-methyladenosine (m6A) is the most prevalent internal modification of eukaryotic RNA and plays a pivotal role in RNA fate. RNA m6A modification is [...] Read more.
Epitranscriptomic RNA modifications play a crucial role in the posttranscriptional regulation of gene expression. N6-methyladenosine (m6A) is the most prevalent internal modification of eukaryotic RNA and plays a pivotal role in RNA fate. RNA m6A modification is regulated by a group of cellular proteins, methyltransferases (writers) and demethylases (erasers), which add and remove the methyl group from adenosine, respectively. m6A modification is recognized by a group of cellular RNA-binding proteins (readers) that specifically bind to m6A-modified RNA, mediating effects on RNA stability, splicing, transport, and translation. The functional significance of m6A modification of viral and cellular RNA is an active area of virology research. In this review, we summarize and analyze the current literature on m6A modification of HIV-1 RNA, the multifaceted functions of m6A in regulating HIV-1 replication, and the role of viral RNA m6A modification in evading innate immune responses to infection. Furthermore, we briefly discuss the future directions and therapeutic implications of mechanistic studies of HIV-1 epitranscriptomic modifications. Full article
(This article belongs to the Special Issue Epigenetic Modifications in Viral Infections)
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Other

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10 pages, 266 KiB  
Perspective
Influenza A Virus and Acetylation: The Picture Is Becoming Clearer
by Matloob Husain
Viruses 2024, 16(1), 131; https://doi.org/10.3390/v16010131 - 17 Jan 2024
Cited by 1 | Viewed by 2515
Abstract
Influenza A virus (IAV) is one of the most circulated human pathogens, and influenza disease, commonly known as the flu, remains one of the most recurring and prevalent infectious human diseases globally. IAV continues to challenge existing vaccines and antiviral drugs via its [...] Read more.
Influenza A virus (IAV) is one of the most circulated human pathogens, and influenza disease, commonly known as the flu, remains one of the most recurring and prevalent infectious human diseases globally. IAV continues to challenge existing vaccines and antiviral drugs via its ability to evolve constantly. It is critical to identify the molecular determinants of IAV pathogenesis to understand the basis of flu severity in different populations and design improved antiviral strategies. In recent years, acetylation has been identified as one of the determinants of IAV pathogenesis. Acetylation was originally discovered as an epigenetic protein modification of histones. But, it is now known to be one of the ubiquitous protein modifications of both histones and non-histone proteins and a determinant of proteome complexity. Since our first observation in 2007, significant progress has been made in understanding the role of acetylation during IAV infection. Now, it is becoming clearer that acetylation plays a pro-IAV function via at least three mechanisms: (1) by reducing the host’s sensing of IAV infection, (2) by dampening the host’s innate antiviral response against IAV, and (3) by aiding the stability and function of viral and host proteins during IAV infection. In turn, IAV antagonizes the host deacetylases, which erase acetylation, to facilitate its replication. This review provides an overview of the research progress made on this subject so far and outlines research prospects for the significance of IAV-acetylation interplay. Full article
(This article belongs to the Special Issue Epigenetic Modifications in Viral Infections)
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