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Viruses
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Varicella Zoster Virus
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Varicella Zoster Virus

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

Deadline for manuscript submissions: closed (30 April 2019) | Viewed by 47235

Special Issue Editor

Prof. Dr. Randall J. Cohrs
*
E-Mail Website
Guest Editor
Department of Neurology, School of Medicine, University of Colorado, Aurora, CO 80045, USA
Interests: molecular biology of alphaherpesvirus latency, especially epigenetic control of latent virus transcription; novel application of next-generation sequencing to questions in virology; reactivation of alphaherpesviruses in extreme environments
* Deceased

Special Issue Information

Dear Colleagues,

With recent advances in vaccine development, disease modeling and global analysis of nucleic acids, proteins, and metabolites, our understanding of the molecular biology of varicella zoster virus (VZV) has expanded.  In addition, application of novel diagnostic tools has expanded the spectrum of disease caused by this virus.  While disease caused by primary infection is still a concern, the larger problem is disease caused when latent VZV reactivates. Consequently, a great deal of current research is directed towards understanding the molecular biology of latency, including host innate and adaptive control of virus reactivation.  This Special Issue is designed to provide a firm base of understanding concerning VZV latency, the mechanism of virus reactivation including the spectrum of disease caused upon reactivation, especially in the expanding elderly and immunocompromised population.  In addition, current treatments including vaccines will be reviewed. 

The goal of this Special Issue is to assemble comprehensive reviews of VZV latency including the latent state, mechanism of reactivation, in vitro and in vivo models, immunology, vaccines, clinical aspects of virus reactivation, and therapy.  It is our hope that this up-to-date review will aid in directing future studies of this enigmatic human alphaherpesvirus.

Prof. Dr. Randall J. Cohrs
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

  • varicella zoster virus
  • human herpesvirus type 3
  • VZV
  • latency
  • reactivation
  • models
  • immunology
  • vaccines
  • disease
  • therapy
  • DNA-seq
  • RNA-seq
  • metabolomics

Published Papers (4 papers)

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Review

25 pages, 2492 KiB  
Review
Current In Vivo Models of Varicella-Zoster Virus Neurotropism
by Ravi Mahalingam, Anne Gershon, Michael Gershon, Jeffrey I. Cohen, Ann Arvin, Leigh Zerboni, Hua Zhu, Wayne Gray, Ilhem Messaoudi and Vicki Traina-Dorge
Viruses 2019, 11(6), 502; https://doi.org/10.3390/v11060502 - 31 May 2019
Cited by 28 | Viewed by 5371
Abstract
Varicella-zoster virus (VZV), an exclusively human herpesvirus, causes chickenpox and establishes a latent infection in ganglia, reactivating decades later to produce zoster and associated neurological complications. An understanding of VZV neurotropism in humans has long been hampered by the lack of an adequate [...] Read more.
Varicella-zoster virus (VZV), an exclusively human herpesvirus, causes chickenpox and establishes a latent infection in ganglia, reactivating decades later to produce zoster and associated neurological complications. An understanding of VZV neurotropism in humans has long been hampered by the lack of an adequate animal model. For example, experimental inoculation of VZV in small animals including guinea pigs and cotton rats results in the infection of ganglia but not a rash. The severe combined immune deficient human (SCID-hu) model allows the study of VZV neurotropism for human neural sub-populations. Simian varicella virus (SVV) infection of rhesus macaques (RM) closely resembles both human primary VZV infection and reactivation, with analyses at early times after infection providing valuable information about the extent of viral replication and the host immune responses. Indeed, a critical role for CD4 T-cell immunity during acute SVV infection as well as reactivation has emerged based on studies using RM. Herein we discuss the results of efforts from different groups to establish an animal model of VZV neurotropism. Full article
(This article belongs to the Special Issue Varicella Zoster Virus)
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15 pages, 2612 KiB  
Review
Current In Vitro Models to Study Varicella Zoster Virus Latency and Reactivation
by Nicholas L. Baird, Shuyong Zhu, Catherine M. Pearce and Abel Viejo-Borbolla
Viruses 2019, 11(2), 103; https://doi.org/10.3390/v11020103 - 26 Jan 2019
Cited by 20 | Viewed by 9884
Abstract
Varicella zoster virus (VZV) is a highly prevalent human pathogen that causes varicella (chicken pox) during primary infection and establishes latency in peripheral neurons. Symptomatic reactivation often presents as zoster (shingles), but it has also been linked to life-threatening diseases such as encephalitis, [...] Read more.
Varicella zoster virus (VZV) is a highly prevalent human pathogen that causes varicella (chicken pox) during primary infection and establishes latency in peripheral neurons. Symptomatic reactivation often presents as zoster (shingles), but it has also been linked to life-threatening diseases such as encephalitis, vasculopathy and meningitis. Zoster may be followed by postherpetic neuralgia, neuropathic pain lasting after resolution of the rash. The mechanisms of varicella zoster virus (VZV) latency and reactivation are not well characterized. This is in part due to the human-specific nature of VZV that precludes the use of most animal and animal-derived neuronal models. Recently, in vitro models of VZV latency and reactivation using human neurons derived from stem cells have been established facilitating an understanding of the mechanisms leading to VZV latency and reactivation. From the models, c-Jun N-terminal kinase (JNK), phosphoinositide 3-kinase (PI3K) and nerve growth factor (NGF) have all been implicated as potential modulators of VZV latency/reactivation. Additionally, it was shown that the vaccine-strain of VZV is impaired for reactivation. These models may also aid in the generation of prophylactic and therapeutic strategies to treat VZV-associated pathologies. This review summarizes and analyzes the current human neuronal models used to study VZV latency and reactivation, and provides some strategies for their improvement. Full article
(This article belongs to the Special Issue Varicella Zoster Virus)
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11 pages, 223 KiB  
Review
Clinical Features of Varicella-Zoster Virus Infection
by Peter G. E. Kennedy and Anne A. Gershon
Viruses 2018, 10(11), 609; https://doi.org/10.3390/v10110609 - 02 Nov 2018
Cited by 181 | Viewed by 19596
Abstract
Varicella-zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (chickenpox) as a primary infection, following which it becomes latent in peripheral ganglia. Decades later, the virus may reactivate either spontaneously or after a number of triggering factors to cause herpes [...] Read more.
Varicella-zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (chickenpox) as a primary infection, following which it becomes latent in peripheral ganglia. Decades later, the virus may reactivate either spontaneously or after a number of triggering factors to cause herpes zoster (shingles). Varicella and its complications are more severe in the immunosuppressed. The most frequent and important complication of VZV reactivation is postherpetic neuralgia, the cause of which is unknown and for which treatment is usually ineffective. Reactivation of VZV may also cause a wide variety of neurological syndromes, the most significant of which is a vasculitis, which is treated with corticosteroids and the antiviral drug acyclovir. Other VZV reactivation complications include an encephalitis, segmental motor weakness and myelopathy, cranial neuropathies, Guillain–Barré syndrome, enteric features, and zoster sine herpete, in which the viral reactivation occurs in the absence of the characteristic dermatomally distributed vesicular rash of herpes zoster. There has also been a recent association of VZV with giant cell arteritis and this interesting finding needs further corroboration. Vaccination is now available for the prevention of both varicella in children and herpes zoster in older individuals. Full article
(This article belongs to the Special Issue Varicella Zoster Virus)
21 pages, 3266 KiB  
Review
Molecular Aspects of Varicella-Zoster Virus Latency
by Daniel P. Depledge, Tomohiko Sadaoka and Werner J. D. Ouwendijk
Viruses 2018, 10(7), 349; https://doi.org/10.3390/v10070349 - 28 Jun 2018
Cited by 50 | Viewed by 11502
Abstract
Primary varicella-zoster virus (VZV) infection causes varicella (chickenpox) and the establishment of a lifelong latent infection in ganglionic neurons. VZV reactivates in about one-third of infected individuals to cause herpes zoster, often accompanied by neurological complications. The restricted host range of VZV and, [...] Read more.
Primary varicella-zoster virus (VZV) infection causes varicella (chickenpox) and the establishment of a lifelong latent infection in ganglionic neurons. VZV reactivates in about one-third of infected individuals to cause herpes zoster, often accompanied by neurological complications. The restricted host range of VZV and, until recently, a lack of suitable in vitro models have seriously hampered molecular studies of VZV latency. Nevertheless, recent technological advances facilitated a series of exciting studies that resulted in the discovery of a VZV latency-associated transcript (VLT) and provide novel insights into our understanding of VZV latency and factors that may initiate reactivation. Deducing the function(s) of VLT and the molecular mechanisms involved should now be considered a priority to improve our understanding of factors that govern VZV latency and reactivation. In this review, we summarize the implications of recent discoveries in the VZV latency field from both a virus and host perspective and provide a roadmap for future studies. Full article
(This article belongs to the Special Issue Varicella Zoster Virus)
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