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Microorganisms
Special Issues
Herpesviruses: Virus-Host Interaction
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Herpesviruses: Virus-Host Interaction

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Virology".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 42607

Special Issue Editor

Dr. Walid Azab

E-Mail Website
Guest Editor
Institut für Virologie, Zentrum für Infektionsmedizin, Freie Universität Berlin, Berlin, Germany
Interests: herpesviruses; virus; herpesvirus–cell interactions; entry; cell-to-cell spread; immune evasion; in vitro models; pathogenesis

Special Issue Information

Dear Colleagues,

Herpesviruses constitute a large family of DNA viruses that can infect a wide variety of species. These viruses not only infect a large diversity of hosts: They also enter and replicate in a broad spectrum of cell types within the same host. The diseases associated with herpesviruses differ but usually range from mild skin lesions, respiratory and reproductive disorders, neurological disorders, to even tumors and death.

The portal of entry is not usually the ultimate goal of hepesviruses. The virus needs to travel (through either blood, represented by immune cells, or nerve) to their preferred tissues where they can establish latency or induce disease. To achieve this goal, different mechanisms of virus–cell interactions have been documented; many are yet to be discovered. Understanding this virus–cell dialogue is the first step toward prevention and control of the infection.

The objective of this Special Issue is to place the spotlight on this branch of research. I cordially invite you to submit your manuscripts (research articles, review articles, and short communications) to this Special Issue: “Herpesviruses: Virus–Host Interaction”. This edition will consider your preferred angle of engagement—whether on virus entry, signaling pathways, cell-to-cell spread, replication, pathogenesis, immune evasion, or in vitro models that facilitate studying virus infection. As Guest Editor of this Special Issue, I look forward to reviewing your submissions and, together, defining the present state of the science.

Dr. Walid Azab
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. Microorganisms 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 2700 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–cell interactions
  • Virus entry
  • Signaling cascades
  • Cell-to-cell spread
  • Immune evasion
  • In vitro models
  • Pathogenesis

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Published Papers (6 papers)

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Research

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16 pages, 2503 KiB  
Article
Equine Alphaherpesviruses Require Activation of the Small GTPases Rac1 and Cdc42 for Intracellular Transport
by Oleksandr Kolyvushko, Maximilian A. Kelch, Nikolaus Osterrieder and Walid Azab
Microorganisms 2020, 8(7), 1013; https://doi.org/10.3390/microorganisms8071013 - 7 Jul 2020
Cited by 8 | Viewed by 3112
Abstract
Viruses utilize host cell signaling to facilitate productive infection. Equine herpesvirus type 1 (EHV-1) has been shown to activate Ca2+ release and phospholipase C upon contact with α4β1 integrins on the cell surface. Signaling molecules, including small GTPases, have been shown to be [...] Read more.
Viruses utilize host cell signaling to facilitate productive infection. Equine herpesvirus type 1 (EHV-1) has been shown to activate Ca2+ release and phospholipase C upon contact with α4β1 integrins on the cell surface. Signaling molecules, including small GTPases, have been shown to be activated downstream of Ca2+ release, and modulate virus entry, membrane remodeling and intracellular transport. In this study, we show that EHV-1 activates the small GTPases Rac1 and Cdc42 during infection. The activation of Rac1 and Cdc42 is necessary for virus-induced acetylation of tubulin, effective viral transport to the nucleus, and cell-to-cell spread. We also show that inhibitors of Rac1 and Cdc42 did not block virus entry, but inhibited overall virus infection. The Rac1 and Cdc42 signaling is presumably orthogonal to Ca2+ release, since Rac1 and Cdc42 inhibitors affected the infection of both EHV-1 and EHV-4, which do not bind to integrins. Full article
(This article belongs to the Special Issue Herpesviruses: Virus-Host Interaction)
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19 pages, 3156 KiB  
Article
Multiple Herpes Simplex Virus-1 (HSV-1) Reactivations Induce Protein Oxidative Damage in Mouse Brain: Novel Mechanisms for Alzheimer’s Disease Progression
by Virginia Protto, Antonella Tramutola, Marco Fabiani, Maria Elena Marcocci, Giorgia Napoletani, Federica Iavarone, Federica Vincenzoni, Massimo Castagnola, Marzia Perluigi, Fabio Di Domenico, Giovanna De Chiara and Anna Teresa Palamara
Microorganisms 2020, 8(7), 972; https://doi.org/10.3390/microorganisms8070972 - 29 Jun 2020
Cited by 19 | Viewed by 3970
Abstract
Compelling evidence supports the role of oxidative stress in Alzheimer’s disease (AD) pathophysiology. Interestingly, Herpes simplex virus-1 (HSV-1), a neurotropic virus that establishes a lifelong latent infection in the trigeminal ganglion followed by periodic reactivations, has been reportedly linked both to AD and [...] Read more.
Compelling evidence supports the role of oxidative stress in Alzheimer’s disease (AD) pathophysiology. Interestingly, Herpes simplex virus-1 (HSV-1), a neurotropic virus that establishes a lifelong latent infection in the trigeminal ganglion followed by periodic reactivations, has been reportedly linked both to AD and to oxidative stress conditions. Herein, we analyzed, through biochemical and redox proteomic approaches, the mouse model of recurrent HSV-1 infection we previously set up, to investigate whether multiple virus reactivations induced oxidative stress in the mouse brain and affected protein function and related intracellular pathways. Following multiple HSV-1 reactivations, we found in mouse brains increased levels of oxidative stress hallmarks, including 4-hydroxynonenal (HNE), and 13 HNE-modified proteins whose levels were found significantly altered in the cortex of HSV-1-infected mice compared to controls. We focused on two proteins previously linked to AD pathogenesis, i.e., glucose-regulated protein 78 (GRP78) and collapsin response-mediated protein 2 (CRMP2), which are involved in the unfolded protein response (UPR) and in microtubule stabilization, respectively. We found that recurrent HSV-1 infection disables GRP78 function and activates the UPR, whereas it prevents CRMP2 function in mouse brains. Overall, these data suggest that repeated HSV-1 reactivation into the brain may contribute to neurodegeneration also through oxidative damage. Full article
(This article belongs to the Special Issue Herpesviruses: Virus-Host Interaction)
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15 pages, 3473 KiB  
Article
Ivermectin Inhibits Bovine Herpesvirus 1 DNA Polymerase Nuclear Import and Interferes With Viral Replication
by Sohail Raza, Farzana Shahin, Wenjun Zhai, Hanxiong Li, Gualtiero Alvisi, Kui Yang, Xi Chen, Yingyu Chen, Jianguo Chen, Changmin Hu, Huanchun Chen and Aizhen Guo
Microorganisms 2020, 8(3), 409; https://doi.org/10.3390/microorganisms8030409 - 13 Mar 2020
Cited by 37 | Viewed by 19096
Abstract
Bovine herpesvirus1 (BoHV-1) is a major bovine pathogen. Despite several vaccines being available to prevent viral infection, outbreaks are frequent and cause important economic consequences worldwide. The development of new antiviral drugs is therefore highly desirable. In this context, viral genome replication represents [...] Read more.
Bovine herpesvirus1 (BoHV-1) is a major bovine pathogen. Despite several vaccines being available to prevent viral infection, outbreaks are frequent and cause important economic consequences worldwide. The development of new antiviral drugs is therefore highly desirable. In this context, viral genome replication represents a potential target for therapeutic intervention. BoHV-1 genome is a dsDNA molecule whose replication takes place in the nuclei of infected cells and is mediated by a viral encoded DNA polymerase holoenzyme. Here, we studied the physical interaction and subcellular localization of BoHV-1 DNA polymerase subunits in cells for the first time. By means of co-immunoprecipitation and confocal laser scanning microscopy (CLSM) experiments, we could show that the processivity factor of the DNA polymerase pUL42 is capable of being autonomously transported into the nucleus, whereas the catalytic subunit pUL30 is not. Accordingly, a putative classic NLS (cNLS) was identified on pUL42 but not on pUL30. Importantly, both proteins could interact in the absence of other viral proteins and their co-expression resulted in accumulation of UL30 to the cell nucleus. Treatment of cells with Ivermectin, an anti-parasitic drug which has been recently identified as an inhibitor of importin α/β-dependent nuclear transport, reduced UL42 nuclear import and specifically reduced BoHV-1 replication in a dose-dependent manner, while virus attachment and entry into cells were not affected. Therefore, this study provides a new option of antiviral therapy for BoHV-1 infection with Ivermectin. Full article
(This article belongs to the Special Issue Herpesviruses: Virus-Host Interaction)
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17 pages, 18979 KiB  
Article
Fatal Elephant Endotheliotropic Herpesvirus Infection of Two Young Asian Elephants
by Selvaraj Pavulraj, Kathrin Eschke, Adriane Prahl, Michael Flügger, Jakob Trimpert, Petra B. van den Doel, Sandro Andreotti, Sabine Kaessmeyer, Nikolaus Osterrieder and Walid Azab
Microorganisms 2019, 7(10), 396; https://doi.org/10.3390/microorganisms7100396 - 26 Sep 2019
Cited by 16 | Viewed by 6423
Abstract
Elephant endotheliotropic herpesvirus (EEHV) can cause a devastating haemorrhagic disease in young Asian elephants worldwide. Here, we report the death of two young Asian elephants after suffering from acute haemorrhagic disease due to EEHV-1A infection. We detected widespread distribution of EEHV-1A in various [...] Read more.
Elephant endotheliotropic herpesvirus (EEHV) can cause a devastating haemorrhagic disease in young Asian elephants worldwide. Here, we report the death of two young Asian elephants after suffering from acute haemorrhagic disease due to EEHV-1A infection. We detected widespread distribution of EEHV-1A in various organs and tissues of the infected elephants. Enveloped viral particles accumulated within and around cytoplasmic electron-dense bodies in hepatic endothelial cells were detected. Attempts to isolate the virus on different cell cultures showed limited virus replication; however, late viral protein expression was detected in infected cells. We further showed that glycoprotein B (gB) of EEHV-1A possesses a conserved cleavage site Arg-X-Lys/Arg-Arg that is targeted by the cellular protease furin, similar to other members of the Herpesviridae. We have determined the complete 180 kb genome sequence of EEHV-1A isolated from the liver by next-generation sequencing and de novo assembly. As virus isolation in vitro has been unsuccessful and limited information is available regarding the function of viral proteins, we have attempted to take the initial steps in the development of suitable cell culture system and virus characterization. In addition, the complete genome sequence of an EEHV-1A in Europe will facilitate future studies on the epidemiology and diagnosis of EEHV infection in elephants. Full article
(This article belongs to the Special Issue Herpesviruses: Virus-Host Interaction)
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Review

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18 pages, 1863 KiB  
Review
The Essential Co-Option of Uracil-DNA Glycosylases by Herpesviruses Invites Novel Antiviral Design
by Renos Savva
Microorganisms 2020, 8(3), 461; https://doi.org/10.3390/microorganisms8030461 - 24 Mar 2020
Cited by 5 | Viewed by 4264
Abstract
Vast evolutionary distances separate the known herpesviruses, adapted to colonise specialised cells in predominantly vertebrate hosts. Nevertheless, the distinct herpesvirus families share recognisably related genomic attributes. The taxonomic Family Herpesviridae includes many important human and animal pathogens. Successful antiviral drugs targeting Herpesviridae are [...] Read more.
Vast evolutionary distances separate the known herpesviruses, adapted to colonise specialised cells in predominantly vertebrate hosts. Nevertheless, the distinct herpesvirus families share recognisably related genomic attributes. The taxonomic Family Herpesviridae includes many important human and animal pathogens. Successful antiviral drugs targeting Herpesviridae are available, but the need for reduced toxicity and improved efficacy in critical healthcare interventions invites novel solutions: immunocompromised patients presenting particular challenges. A conserved enzyme required for viral fitness is Ung, a uracil-DNA glycosylase, which is encoded ubiquitously in Herpesviridae genomes and also host cells. Research investigating Ung in Herpesviridae dynamics has uncovered an unexpected combination of viral co-option of host Ung, along with remarkable Subfamily-specific exaptation of the virus-encoded Ung. These enzymes apparently play essential roles, both in the maintenance of viral latency and during initiation of lytic replication. The ubiquitously conserved Ung active site has previously been explored as a therapeutic target. However, exquisite selectivity and better drug-like characteristics might instead be obtained via targeting structural variations within another motif of catalytic importance in Ung. The motif structure is unique within each Subfamily and essential for viral survival. This unique signature in highly conserved Ung constitutes an attractive exploratory target for the development of novel beneficial therapeutics. Full article
(This article belongs to the Special Issue Herpesviruses: Virus-Host Interaction)
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Other

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9 pages, 1188 KiB  
Brief Report
Marek’s Disease Virus Infection of Natural Killer Cells
by Luca D. Bertzbach, Daphne A. van Haarlem, Sonja Härtle, Benedikt B. Kaufer and Christine A. Jansen
Microorganisms 2019, 7(12), 588; https://doi.org/10.3390/microorganisms7120588 - 20 Nov 2019
Cited by 34 | Viewed by 4724
Abstract
Natural killer (NK) cells are key players in the innate immune response. They kill virus-infected cells and are crucial for the induction of adaptive immune responses. Marek’s disease virus (MDV) is a highly contagious alphaherpesvirus that causes deadly T cell lymphomas in chickens. [...] Read more.
Natural killer (NK) cells are key players in the innate immune response. They kill virus-infected cells and are crucial for the induction of adaptive immune responses. Marek’s disease virus (MDV) is a highly contagious alphaherpesvirus that causes deadly T cell lymphomas in chickens. Host resistance to MDV is associated with differences in NK cell responses; however, the exact role of NK cells in the control of MDV remains unknown. In this study, we assessed if MDV can infect NK cells and alter their activation. Surprisingly, we could demonstrate that primary chicken NK cells are very efficiently infected with very virulent RB-1B MDV and the live-attenuated CVI988 vaccine. Flow cytometry analysis revealed that both RB-1B and CVI988 enhance NK cell degranulation and increase interferon gamma (IFNγ) production in vitro. In addition, we could show that the MDV Eco Q-encoded oncogene (meq) contributes to the induction of NK cell activation using meq knockout viruses. Taken together, our data revealed for the first time that NK cells are efficiently infectable with MDV and that this oncogenic alphaherpesvirus enhances NK cell degranulation and increased IFNγ production in vitro. Full article
(This article belongs to the Special Issue Herpesviruses: Virus-Host Interaction)
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