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Viruses
Special Issues
Epigenetic and Transcriptional Regulation of DNA Virus Infections
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Epigenetic and Transcriptional Regulation of DNA Virus Infections

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 7482

Special Issue Editor

Dr. Zsolt Toth

E-Mail Website
Guest Editor
Department of Oral Biology, University of Florida College of Dentistry, 1395 Center Drive, Gainesville, FL 32610, USA
Interests: epigenetic regulation of the KSHV life cycle; de novo viral infection; the establishment and maintenance of KSHV latency; lytic reactivation from latency

Special Issue Information

Dear Colleagues,

The goal of this Special Issue is to highlight the gene-controlling mechanisms of the viral and host factors involved in the regulation of DNA virus infections. DNA viruses replicating in the nuclei of infected cells have evolved in such a way that they are able to utilize the transcriptional and epigenetic machineries of the host cells to facilitate the viral infection. Both original research and review articles on any DNA viruses that infect humans or the animal kingdom are welcome. We invite primary studies and reviews that deal with any steps of gene expression regulation, including transcriptional, post-transcriptional, and epigenetic mechanisms during primary viral infection, viral latency, or lytic viral reactivation.

Dr. Zsolt Toth
Guest Editor

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 gene regulation
  • DNA virus
  • primary infection
  • latency
  • viral reactivation
  • chromatin regulatory factors
  • epigenetic factors
  • transcriptional gene regulation
  • post-transcriptional gene regulation

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Published Papers (6 papers)

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Research

Jump to: Review, Other

17 pages, 2700 KiB  
Article
Glucocorticoid Receptor (GR) and Specificity Protein 1 (Sp1) or Sp3 Transactivate the Bovine Alphaherpesvirus 1 (BoHV-1)-Infected Cell Protein 0 Early Promoter
by Sankha Hewawasam, Fouad S. El-Mayet and Clinton Jones
Viruses 2025, 17(2), 229; https://doi.org/10.3390/v17020229 - 7 Feb 2025
Viewed by 715
Abstract
Bovine alphaherpesvirus 1 (BoHV-1) acute infection leads to latently infected sensory neurons in trigeminal ganglia. During lytic infection, the immediate early expression of infected cell protein 0 (bICP0) and bICP4 is regulated by an immediate early transcription unit 1 (IEtu1) promoter. A separate [...] Read more.
Bovine alphaherpesvirus 1 (BoHV-1) acute infection leads to latently infected sensory neurons in trigeminal ganglia. During lytic infection, the immediate early expression of infected cell protein 0 (bICP0) and bICP4 is regulated by an immediate early transcription unit 1 (IEtu1) promoter. A separate bICP0 early (E) promoter drives bICP0 as an early viral gene, presumably to sustain high levels during productive infection. Notably, bICP0 protein expression is detected before bICP4 during reactivation from latency, suggesting the bICP0 E promoter drives bICP0 protein expression during the early phases of reactivation from latency. The glucocorticoid receptor (GR) and Krüppel-like factor 4 (KLF4) cooperatively transactivate the bICP0 E promoter despite this promoter lacks a consensus GR response element (GRE). KLF and specificity protein (Sp) family members comprise a “super-family” of transcription factors. Consequently, we hypothesized Sp1 and Sp3 transactivated the bICP0 E promoter. These studies revealed GR and Sp3 or Sp1 cooperatively transactivated bICP0 E promoter activity. KLF4 and Sp3, but not Sp1, had an additive effect on bICP0 E promoter activity. Mutating the consensus Sp1 and CACCC binding sites proximal to the TATA box impaired promoter activity more than the Sp1 sites further upstream from the TATA box. Full article
(This article belongs to the Special Issue Epigenetic and Transcriptional Regulation of DNA Virus Infections)
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25 pages, 5366 KiB  
Article
Characterization of Human Cytomegalovirus (HCMV) Long Non-Coding RNA1.2 During Lytic Replication
by Salomé Manska, Andrew Hagemann, Janna Magana, Cyprian C. Rossetto and Subhash C. Verma
Viruses 2025, 17(2), 149; https://doi.org/10.3390/v17020149 - 23 Jan 2025
Viewed by 735
Abstract
During lytic replication of human cytomegalovirus (HCMV), the most abundant viral transcripts are long non-coding RNAs (lncRNAs). Viral lncRNAs can have a variety of functions, some of which are necessary for viral production and the modulation of host processes during infection. HCMV produces [...] Read more.
During lytic replication of human cytomegalovirus (HCMV), the most abundant viral transcripts are long non-coding RNAs (lncRNAs). Viral lncRNAs can have a variety of functions, some of which are necessary for viral production and the modulation of host processes during infection. HCMV produces four lncRNAs, Beta2.7 (RNA2.7), RNA4.9, RNA5.0 and RNA1.2. While there has been research on these viral lncRNAs, many of their functions remain uncharacterized. To determine the function of RNA1.2, we explored its requirement during lytic infection by generating viral mutants containing either a full or partial deletion of the RNA1.2 locus. Within permissive fibroblasts, the RNA1.2 deletion mutants showed no defects in viral DNA synthesis, transcript expression, protein production, or generation of viral progeny. Further investigation to identify potential cellular and viral protein binding partners of RNA1.2 was performed using liquid chromatography-mass spectrometry (LC-MS). A significant number of cellular proteins were identified and associated with RNA1.2. Specifically those associated with the innate immune response, mitochondrial processes, and cell cycle regulation. While RNA1.2 is dispensable for lytic replication, these findings suggest it may play a pivotal role in modulating the host response. Full article
(This article belongs to the Special Issue Epigenetic and Transcriptional Regulation of DNA Virus Infections)
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17 pages, 2766 KiB  
Article
cGAS-STING-TBK1 Signaling Promotes Valproic Acid-Responsive Human Cytomegalovirus Immediate-Early Transcription during Infection of Incompletely Differentiated Myeloid Cells
by Emily R. Albright and Robert F. Kalejta
Viruses 2024, 16(6), 877; https://doi.org/10.3390/v16060877 - 30 May 2024
Cited by 1 | Viewed by 1503
Abstract
Repression of human cytomegalovirus (HCMV) immediate-early (IE) gene expression is a key regulatory step in the establishment and maintenance of latent reservoirs. Viral IE transcription and protein accumulation can be elevated during latency by treatment with histone deacetylase inhibitors such as valproic acid [...] Read more.
Repression of human cytomegalovirus (HCMV) immediate-early (IE) gene expression is a key regulatory step in the establishment and maintenance of latent reservoirs. Viral IE transcription and protein accumulation can be elevated during latency by treatment with histone deacetylase inhibitors such as valproic acid (VPA), rendering infected cells visible to adaptive immune responses. However, the latency-associated viral protein UL138 inhibits the ability of VPA to enhance IE gene expression during infection of incompletely differentiated myeloid cells that support latency. UL138 also limits the accumulation of IFNβ transcripts by inhibiting the cGAS-STING-TBK1 DNA-sensing pathway. Here, we show that, in the absence of UL138, the cGAS-STING-TBK1 pathway promotes both IFNβ accumulation and VPA-responsive IE gene expression in incompletely differentiated myeloid cells. Inactivation of this pathway by either genetic or pharmacological inhibition phenocopied UL138 expression and reduced VPA-responsive IE transcript and protein accumulation. This work reveals a link between cytoplasmic pathogen sensing and epigenetic control of viral lytic phase transcription and suggests that manipulation of pattern recognition receptor signaling pathways could aid in the refinement of MIEP regulatory strategies to target latent viral reservoirs. Full article
(This article belongs to the Special Issue Epigenetic and Transcriptional Regulation of DNA Virus Infections)
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22 pages, 8868 KiB  
Article
Genome-Wide Transcriptional Roles of KSHV Viral Interferon Regulatory Factors in Oral Epithelial Cells
by Seung Jin Jang, Natalie Atyeo, Mario Mietzsch, Min Y. Chae, Robert McKenna, Zsolt Toth and Bernadett Papp
Viruses 2024, 16(6), 846; https://doi.org/10.3390/v16060846 - 25 May 2024
Viewed by 1378
Abstract
The viral interferon regulatory factors (vIRFs) of KSHV are known to dysregulate cell signaling pathways to promote viral oncogenesis and to block antiviral immune responses to facilitate infection. However, it remains unknown to what extent each vIRF plays a role in gene regulation. [...] Read more.
The viral interferon regulatory factors (vIRFs) of KSHV are known to dysregulate cell signaling pathways to promote viral oncogenesis and to block antiviral immune responses to facilitate infection. However, it remains unknown to what extent each vIRF plays a role in gene regulation. To address this, we performed a comparative analysis of the protein structures and gene regulation of the four vIRFs. Our structure prediction analysis revealed that despite their low amino acid sequence similarity, vIRFs exhibit high structural homology in both their DNA-binding domain (DBD) and IRF association domain. However, despite this shared structural homology, we demonstrate that each vIRF regulates a distinct set of KSHV gene promoters and human genes in epithelial cells. We also found that the DBD of vIRF1 is essential in regulating the expression of its target genes. We propose that the structurally similar vIRFs evolved to possess specialized transcriptional functions to regulate specific genes. Full article
(This article belongs to the Special Issue Epigenetic and Transcriptional Regulation of DNA Virus Infections)
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Review

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21 pages, 720 KiB  
Review
Rewriting Viral Fate: Epigenetic and Transcriptional Dynamics in KSHV Infection
by Chunyan Han, Danping Niu and Ke Lan
Viruses 2024, 16(12), 1870; https://doi.org/10.3390/v16121870 - 30 Nov 2024
Cited by 1 | Viewed by 1231
Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV), a γ-herpesvirus, is predominantly associated with Kaposi’s sarcoma (KS) as well as two lymphoproliferative disorders: primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). Like other herpesviruses, KSHV employs two distinct life cycles: latency and lytic replication. To establish [...] Read more.
Kaposi’s sarcoma-associated herpesvirus (KSHV), a γ-herpesvirus, is predominantly associated with Kaposi’s sarcoma (KS) as well as two lymphoproliferative disorders: primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). Like other herpesviruses, KSHV employs two distinct life cycles: latency and lytic replication. To establish a lifelong persistent infection, KSHV has evolved various strategies to manipulate the epigenetic machinery of the host. In latently infected cells, most viral genes are epigenetically silenced by components of cellular chromatin, DNA methylation and histone post-translational modifications. However, some specific latent genes are preserved and actively expressed to maintain the virus’s latent state within the host cell. Latency is not a dead end, but the virus has the ability to reactivate. This reactivation is a complex process that involves the removal of repressive chromatin modifications and increased accessibility for both viral and cellular factors, allowing the activation of the full transcriptional program necessary for the subsequent lytic replication. This review will introduce the roles of epigenetic modifications in KSHV latent and lytic life cycles, including DNA methylation, histone methylation and acetylation modifications, chromatin remodeling, genome conformation, and non-coding RNA expression. Additionally, we will also review the transcriptional regulation of viral genes and host factors in KSHV infection. This review aims to enhance our understanding of the molecular mechanisms of epigenetic modifications and transcriptional regulation in the KSHV life cycle, providing insights for future research. Full article
(This article belongs to the Special Issue Epigenetic and Transcriptional Regulation of DNA Virus Infections)
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Other

Jump to: Research, Review

11 pages, 578 KiB  
Opinion
Targeting EBV Episome for Anti-Cancer Therapy: Emerging Strategies and Challenges
by Febri Gunawan Sugiokto and Renfeng Li
Viruses 2025, 17(1), 110; https://doi.org/10.3390/v17010110 - 15 Jan 2025
Viewed by 1279
Abstract
As a ubiquitous human pathogen, the Epstein–Barr virus (EBV) has established lifelong persistent infection in about 95% of the adult population. The EBV infection is associated with approximately 200,000 human cancer cases and 140,000 deaths per year. The presence of EBV in tumor [...] Read more.
As a ubiquitous human pathogen, the Epstein–Barr virus (EBV) has established lifelong persistent infection in about 95% of the adult population. The EBV infection is associated with approximately 200,000 human cancer cases and 140,000 deaths per year. The presence of EBV in tumor cells provides a unique advantage in targeting the viral genome (also known as episome), to develop anti-cancer therapeutics. In this review, we summarize current strategies targeting the viral episome in cancer cells. We also highlight emerging technologies, such as clustered regularly interspersed short palindromic repeat (CRISPR)-based gene editing or activation, which offer promising avenues for selective targeting of the EBV episome for anti-cancer therapy. We discuss the challenges, limitations, and future perspectives associated with these strategies, including potential off-target effects, anti-cancer efficacy and safety. Full article
(This article belongs to the Special Issue Epigenetic and Transcriptional Regulation of DNA Virus Infections)
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