Special Issue "Replication and Spread of Alphaherpesviruses"

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

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editor

Prof. Dr. Stephen A. Rice
E-Mail Website
Guest Editor
Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN, USA
Interests: Herpes simplex virus type-1 (HSV-1); viral gene expression; immediate-early proteins; post-transcriptional gene regulation; viral spread

Special Issue Information

Dear Colleagues,

Alphaherpesviruses comprise one of the three subfamilies of the Herpesviridae, a large group of nuclear-replicating, double-stranded DNA viruses that infect mammalian, avian, and reptilian species. This subfamily includes important human pathogens such as Herpes simplex virus types 1 and 2 and Varicella-zoster virus, as well as veterinary pathogens including Marek’s disease virus and Pseuodorabies virus. Similar to all other viruses, alphaherpesviruses must carry out the fundamental steps of the viral infectious cycle in order to replicate in their host cells. These steps include (but are not limited to) receptor-mediated cell entry, gene expression, genome replication, virion assembly, and particle egress. In addition, in order to propagate themselves in nature, progeny alphaherpesvirus particles must efficiently spread to new target cells in an infected host as well as to naive individuals in a host population. This Special Issue focuses on new and emerging findings relevant to the fundamental mechanisms that alphaherpesviruses use to replicate and spread in their host species. Such knowledge is important, not only to more fully understand these fascinating forms of life but also to develop novel strategies to prevent or limit the diseases that they cause.

Prof. Dr. Stephen A. Rice
Guest Editor

Manuscript Submission Information

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Keywords

  • alphaherpesviruses
  • HSV-1
  • HSV-1
  • VZV
  • MDV
  • PRV
  • cell entry
  • viral gene expression
  • viral DNA replication
  • virion assembly
  • viral egress
  • viral spread
  • horizontal transmission

Published Papers (2 papers)

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Research

Article
The Requirement of Glycoprotein C for Interindividual Spread Is Functionally Conserved within the Alphaherpesvirus Genus (Mardivirus), but Not the Host (Gallid)
Viruses 2021, 13(8), 1419; https://doi.org/10.3390/v13081419 - 21 Jul 2021
Viewed by 373
Abstract
Marek’s disease (MD) in chickens is caused by Gallid alphaherpesvirus 2, better known as MD herpesvirus (MDV). Current vaccines do not block interindividual spread from chicken-to-chicken, therefore, understanding MDV interindividual spread provides important information for the development of potential therapies to protect against [...] Read more.
Marek’s disease (MD) in chickens is caused by Gallid alphaherpesvirus 2, better known as MD herpesvirus (MDV). Current vaccines do not block interindividual spread from chicken-to-chicken, therefore, understanding MDV interindividual spread provides important information for the development of potential therapies to protect against MD, while also providing a natural host to study herpesvirus dissemination. It has long been thought that glycoprotein C (gC) of alphaherpesviruses evolved with their host based on their ability to bind and inhibit complement in a species-selective manner. Here, we tested the functional importance of gC during interindividual spread and host specificity using the natural model system of MDV in chickens through classical compensation experiments. By exchanging MDV gC with another chicken alphaherpesvirus (Gallid alphaherpesvirus 1 or infectious laryngotracheitis virus; ILTV) gC, we determined that ILTV gC could not compensate for MDV gC during interindividual spread. In contrast, exchanging turkey herpesvirus (Meleagrid alphaherpesvirus 1 or HVT) gC could compensate for chicken MDV gC. Both ILTV and MDV are Gallid alphaherpesviruses; however, ILTV is a member of the Iltovirus genus, while MDV is classified as a Mardivirus along with HVT. These results suggest that gC is functionally conserved based on the virus genera (Mardivirus vs. Iltovirus) and not the host (Gallid vs. Meleagrid). Full article
(This article belongs to the Special Issue Replication and Spread of Alphaherpesviruses)
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Article
Histopathological Analysis of Adrenal Glands after Simian Varicella Virus Infection
Viruses 2021, 13(7), 1245; https://doi.org/10.3390/v13071245 - 26 Jun 2021
Viewed by 652
Abstract
Latent varicella zoster virus (VZV) has been detected in human adrenal glands, raising the possibility of virus-induced adrenal damage and dysfunction during primary infection or reactivation. Rare cases of bilateral adrenal hemorrhage and insufficiency associated with VZV reactivation have been reported. Since there [...] Read more.
Latent varicella zoster virus (VZV) has been detected in human adrenal glands, raising the possibility of virus-induced adrenal damage and dysfunction during primary infection or reactivation. Rare cases of bilateral adrenal hemorrhage and insufficiency associated with VZV reactivation have been reported. Since there is no animal model for VZV infection of adrenal glands, we obtained adrenal glands from two non-human primates (NHPs) that spontaneously developed varicella from primary simian varicella virus (SVV) infection, the NHP VZV homolog. Histological and immunohistochemical analysis revealed SVV antigen and DNA in the adrenal medulla and cortex of both animals. Adrenal glands were observed to have Cowdry A inclusion bodies, cellular necrosis, multiple areas of hemorrhage, and varying amounts of polymorphonuclear cells. No specific association of SVV antigen with βIII-tubulin-positive nerve fibers was found. Overall, we found that SVV can productively infect NHP adrenal glands, and is associated with inflammation, hemorrhage, and cell death. These findings suggest that further studies are warranted to examine the contribution of VZV infection to human adrenal disease. This study also suggests that VZV infection may present itself as acute adrenal dysfunction with “long-hauler” symptoms of fatigue, weakness, myalgias/arthralgias, and hypotension. Full article
(This article belongs to the Special Issue Replication and Spread of Alphaherpesviruses)
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