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Viruses
Special Issues
Herpesvirus Manipulation of Cellular Processes
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Herpesvirus Manipulation of Cellular Processes

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

Deadline for manuscript submissions: closed (16 April 2021) | Viewed by 20293

Special Issue Editors

Dr. Magdalena Weidner-Glunde

E-Mail Website
Guest Editor
Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences in Olsztyn, Tuwima 10, 10-748 Olsztyn, Poland
Interests: molecular virology; virus-host interactions; cell biology of viral infections; herpesviruses; Kaposi's sarcoma-associated herpesvirus; latency-associated nuclear antigen; immunity; human cytomegalovirus; congenital infections
Special Issues, Collections and Topics in MDPI journals
Dr. Andrea Lipińska

E-Mail Website
Guest Editor
Department of Virus Molecular Biology, Intercollegiate Faculty of Biotechnology, University of Gdańsk and Medical University of Gdańsk, Abrahama 58, 80-307 Gdańsk, Poland
Interests: molecular virology; alphaherpesviruses; viral vectors; immune evasion (innate immunity and antigen presentation); cell biology of viral infections; endosomal traffcking; autophagy; extracellular vesicles; virus-encoded miRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

All viruses influence cellular processes upon infection, but herpesviruses are absolute masters in tweaking the cellular processes to their advantage. Like many other viruses, they infect cells and practically convert them into virus-producing factories, keeping and enhancing the cell functions that are needed for viral replication and particle production and suppressing those that could inhibit the successful completion of the productive viral cycle. Additionally, due to the establishment of latency, hallmark of this virus family, they have developed additional “tools” to manipulate cellular factors over long periods of time without causing cellular death. This Special Issue of Viruses will focus on how herpesviruses influence cellular processes and what consequences this modulation has both for the cell and for the virus.

Dr. Magdalena Weidner-Glunde
Dr. Andrea Lipińska
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

  • herpesvirus
  • virus–host interaction
  • latency
  • lytic replication
  • immune evasion
  • molecular piracy
  • signaling pathways
  • host shutoff
  • modulation of intracellular trafficking of molecules
  • modulation of autophagy
  • modulation of cell death processes

Published Papers (6 papers)

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Research

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13 pages, 3043 KiB  
Article
Regulation of Krüppel-Like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection
by Fouad S. El-mayet, Kelly S. Harrison and Clinton Jones
Viruses 2021, 13(6), 1148; https://doi.org/10.3390/v13061148 - 15 Jun 2021
Cited by 6 | Viewed by 2313
Abstract
Expression of Krüppel-like factor 15 (KLF15), a stress-induced transcription factor, is induced during bovine herpesvirus 1 (BoHV-1) reactivation from latency, and KLF15 stimulates BoHV-1 replication. Transient transfection studies revealed that KLF15 and glucocorticoid receptor (GR) cooperatively transactivate the BoHV-1-immediate-early transcription unit 1 (IEtu1), [...] Read more.
Expression of Krüppel-like factor 15 (KLF15), a stress-induced transcription factor, is induced during bovine herpesvirus 1 (BoHV-1) reactivation from latency, and KLF15 stimulates BoHV-1 replication. Transient transfection studies revealed that KLF15 and glucocorticoid receptor (GR) cooperatively transactivate the BoHV-1-immediate-early transcription unit 1 (IEtu1), herpes simplex virus type 1 (HSV-1) infected cell protein 0 (ICP0), and ICP4 promoters. The IEtu1 promoter drives expression of bICP0 and bICP4, two key BoHV-1 transcriptional regulatory proteins. Based on these studies, we hypothesized infection is a stressful stimulus that increases KLF15 expression and enhances productive infection. New studies demonstrated that silencing KLF15 impaired HSV-1 productive infection, and KLF15 steady-state protein levels were increased at late stages of productive infection. KLF15 was primarily localized to the nucleus following infection of cultured cells with HSV-1, but not BoHV-1. When cells were transfected with a KLF15 promoter construct and then infected with HSV-1, promoter activity was significantly increased. The ICP0 gene, and to a lesser extent, bICP0 transactivated the KLF15 promoter in the absence of other viral proteins. In contrast, BoHV-1 or HSV-1 encoded VP16 had no effect on KLF15 promoter activity. Collectively, these studies revealed that HSV-1 and BoHV-1 productive infection increased KLF15 steady-state protein levels, which correlated with increased virus production. Full article
(This article belongs to the Special Issue Herpesvirus Manipulation of Cellular Processes)
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14 pages, 1129 KiB  
Article
Pseudorabies Virus Infection Causes Downregulation of Ligands for the Activating NK Cell Receptor NKG2D
by Sofie Denaeghel, Steffi De Pelsmaeker, Cliff Van Waesberghe and Herman W. Favoreel
Viruses 2021, 13(2), 266; https://doi.org/10.3390/v13020266 - 9 Feb 2021
Cited by 4 | Viewed by 2025
Abstract
Herpesviruses display a complex and carefully balanced interaction with important players in the antiviral immune response of immunocompetent natural hosts, including natural killer (NK) cells. With regard to NK cells, this delicate balance is illustrated on the one hand by severe herpesvirus disease [...] Read more.
Herpesviruses display a complex and carefully balanced interaction with important players in the antiviral immune response of immunocompetent natural hosts, including natural killer (NK) cells. With regard to NK cells, this delicate balance is illustrated on the one hand by severe herpesvirus disease reported in individuals with NK cell deficiencies and on the other hand by several NK cell evasion strategies described for herpesviruses. In the current study, we report that porcine cells infected with the porcine alphaherpesvirus pseudorabies virus (PRV) display a rapid and progressive downregulation of ligands for the major activating NK cell receptor NKG2D. This downregulation consists both of a downregulation of NKG2D ligands that are already expressed on the cell surface of an infected cell and an inhibition of cell surface expression of newly expressed NKG2D ligands. Flow cytometry and RT-qPCR assays showed that PRV infection results in downregulation of the porcine NKG2D ligand pULBP1 from the cell surface and a very substantial suppression of mRNA expression of pULBP1 and of another potential NKG2D ligand, pMIC2. Furthermore, PRV-induced NKG2D ligand downregulation was found to be independent of late viral gene expression. In conclusion, we report that PRV infection of host cells results in a very pronounced downregulation of ligands for the activating NK cell receptor NKG2D, representing an additional NK evasion strategy of PRV. Full article
(This article belongs to the Special Issue Herpesvirus Manipulation of Cellular Processes)
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17 pages, 5632 KiB  
Article
UBE1a Suppresses Herpes Simplex Virus-1 Replication
by Marina Ikeda, Akihiro Ito, Yuichi Sekine and Masahiro Fujimuro
Viruses 2020, 12(12), 1391; https://doi.org/10.3390/v12121391 - 4 Dec 2020
Cited by 3 | Viewed by 2578
Abstract
Herpes simplex virus-1 (HSV-1) is the causative agent of cold sores, keratitis, meningitis, and encephalitis. HSV-1-encoded ICP5, the major capsid protein, is essential for capsid assembly during viral replication. Ubiquitination is a post-translational modification that plays a critical role in the regulation of [...] Read more.
Herpes simplex virus-1 (HSV-1) is the causative agent of cold sores, keratitis, meningitis, and encephalitis. HSV-1-encoded ICP5, the major capsid protein, is essential for capsid assembly during viral replication. Ubiquitination is a post-translational modification that plays a critical role in the regulation of cellular events such as proteasomal degradation, protein trafficking, and the antiviral response and viral events such as the establishment of infection and viral replication. Ub-activating enzyme (E1, also named UBE1) is involved in the first step in the ubiquitination. However, it is still unknown whether UBE1 contributes to viral infection or the cellular antiviral response. Here, we found that UBE1a suppressed HSV-1 replication and contributed to the antiviral response. The UBE1a inhibitor PYR-41 increased HSV-1 production. Immunofluorescence analysis revealed that UBE1a highly expressing cells presented low ICP5 expression, and vice versa. UBE1a inhibition by PYR-41 and shRNA increased ICP5 expression in HSV-1-infected cells. UBE1a reduced and retarded ICP5 protein expression, without affecting transcription of ICP5 mRNA or degradation of ICP5 protein. Additionally, UBE1a interacted with ICP27, and both partially co-localized at the Hsc70 foci/virus-induced chaperone-enriched (VICE) domains. PYR-41 reduced the co-localization of UBE1a and ICP27. Thus, our findings provide insights into the mechanism of UBE1a in the cellular response to viral infection. Full article
(This article belongs to the Special Issue Herpesvirus Manipulation of Cellular Processes)
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Review

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13 pages, 1462 KiB  
Review
Regulation of the Macroautophagic Machinery, Cellular Differentiation, and Immune Responses by Human Oncogenic γ-Herpesviruses
by Christian Münz
Viruses 2021, 13(5), 859; https://doi.org/10.3390/v13050859 - 8 May 2021
Viewed by 2324
Abstract
The human γ-herpesviruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) encode oncogenes for B cell transformation but are carried by most infected individuals without symptoms. For this purpose, they manipulate the anti-apoptotic pathway macroautophagy, cellular proliferation and apoptosis, as well as immune [...] Read more.
The human γ-herpesviruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) encode oncogenes for B cell transformation but are carried by most infected individuals without symptoms. For this purpose, they manipulate the anti-apoptotic pathway macroautophagy, cellular proliferation and apoptosis, as well as immune recognition. The mechanisms and functional relevance of these manipulations are discussed in this review. They allow both viruses to strike the balance between efficient persistence and dissemination in their human hosts without ever being cleared after infection and avoiding pathologies in most of their carriers. Full article
(This article belongs to the Special Issue Herpesvirus Manipulation of Cellular Processes)
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15 pages, 707 KiB  
Review
Herpesvirus Regulation of Selective Autophagy
by Mai Tram Vo and Young Bong Choi
Viruses 2021, 13(5), 820; https://doi.org/10.3390/v13050820 - 1 May 2021
Cited by 6 | Viewed by 3831
Abstract
Selective autophagy has emerged as a key mechanism of quality and quantity control responsible for the autophagic degradation of specific subcellular organelles and materials. In addition, a specific type of selective autophagy (xenophagy) is also activated as a line of defense against invading [...] Read more.
Selective autophagy has emerged as a key mechanism of quality and quantity control responsible for the autophagic degradation of specific subcellular organelles and materials. In addition, a specific type of selective autophagy (xenophagy) is also activated as a line of defense against invading intracellular pathogens, such as viruses. However, viruses have evolved strategies to counteract the host’s antiviral defense and even to activate some proviral types of selective autophagy, such as mitophagy, for their successful infection and replication. This review discusses the current knowledge on the regulation of selective autophagy by human herpesviruses. Full article
(This article belongs to the Special Issue Herpesvirus Manipulation of Cellular Processes)
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16 pages, 844 KiB  
Review
The Role of Congenital Cytomegalovirus Infection in Adverse Birth Outcomes: A Review of the Potential Mechanisms
by Annete Njue, Carolyn Coyne, Andrea V. Margulis, Dai Wang, Morgan A. Marks, Kevin Russell, Rituparna Das and Anushua Sinha
Viruses 2021, 13(1), 20; https://doi.org/10.3390/v13010020 - 24 Dec 2020
Cited by 27 | Viewed by 6477
Abstract
Human cytomegalovirus (CMV) is a major cause of nonhereditary adverse birth outcomes, including hearing and visual loss, neurologic deficits, and intrauterine growth retardation (IUGR), and may contribute to outcomes such as stillbirth and preterm delivery. However, the mechanisms by which CMV could cause [...] Read more.
Human cytomegalovirus (CMV) is a major cause of nonhereditary adverse birth outcomes, including hearing and visual loss, neurologic deficits, and intrauterine growth retardation (IUGR), and may contribute to outcomes such as stillbirth and preterm delivery. However, the mechanisms by which CMV could cause adverse birth outcomes are not fully understood. This study reviewed proposed mechanisms underlying the role of CMV in stillbirth, preterm birth, and IUGR. Targeted literature searches were performed in PubMed and Embase to identify relevant articles. Several potential mechanisms were identified from in vitro studies in which laboratory-adapted and low-passage strains of CMV and various human placental models were used. Potential mechanisms identified included impairment of trophoblast progenitor stem cell differentiation and function, impairment of extravillous trophoblast invasiveness, dysregulation of Wnt signaling pathways in cytotrophoblasts, tumor necrosis factor-α mediated apoptosis of trophoblasts, CMV-induced cytokine changes in the placenta, inhibition of indoleamine 2,3-dioxygenase activity, and downregulation of trophoblast class I major histocompatibility complex molecules. Inherent challenges for the field remain in the identification of suitable in vivo animal models. Nonetheless, we believe that our review provides useful insights into the mechanisms by which CMV impairs placental development and function and how these changes could result in adverse birth outcomes. Full article
(This article belongs to the Special Issue Herpesvirus Manipulation of Cellular Processes)
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