Marek's Disease Virus

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 761

Special Issue Editors


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Guest Editor
Department of Pathobiology, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, IL 61802, USA
Interests: herpesvirus replication; pathogenesis; transmission and transformation

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Guest Editor
Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA
Interests: DNA virus replication and pathogenesis

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Guest Editor
Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA
Interests: virus infection; innate immune responses to virus infection

Special Issue Information

Dear Colleagues,

Marek’s disease (MD) virus (MDV) has caused major problems worldwide. It is a highly contagious herpesvirus that causes cancer in poultry species, primarily chickens. It is a member of the Alphaherpesvirinae within the Orthoherpesviridae family with similar replicative properties to other alphaherpesviruses like human herpes simplex (HSV) and varicella zoster (VZV) viruses that spread through shedding from epithelial skin cells. However, within the host, its pathogenesis is more similar to gammaherpesviruses with its lymphotropic nature, and like Epstein-Barr (EBV) and Kaposi-sarcoma-associated (KSHV) viruses, transform lymphocytes inducing cancer. Research on MDV has produced tremendous knowledge of virus-induced disease and cancer, and transmission from host to host over the decades. However, there are still significant gaps in knowledge in understanding the viral and host factors that contribute to virus replication, transformation, and transmission. In addition, information about how homologous vaccines are used to protect chickens from MDV-induced disease and understanding the mechanistic importance these vaccines play are needed to develop new vaccines and antiviral strategies. This Special Issue will focus on articles that provide deeper insights into important aspects of MDV and related MD vaccines, lytic replication, latency, transformation, reactivation, pathogenesis, and immune system interactions.

Dr. Keith Jarosinski
Dr. Nagendraprabhu Ponnuraj
Dr. Haji Akbar
Guest Editors

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Keywords

  • Marek’s disease virus (MDV)
  • poultry
  • herpesvirus
  • cancer
  • transmission
  • pathogenesis

Published Papers (1 paper)

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Research

14 pages, 3743 KiB  
Article
mRNA Splicing of UL44 and Secretion of Alphaherpesvirinae Glycoprotein C (gC) Is Conserved among the Mardiviruses
by Huai Xu, Widaliz Vega-Rodriguez, Valeria Campos and Keith W. Jarosinski
Viruses 2024, 16(5), 782; https://doi.org/10.3390/v16050782 - 15 May 2024
Viewed by 445
Abstract
Marek’s disease (MD), caused by gallid alphaherpesvirus 2 (GaAHV2) or Marek’s disease herpesvirus (MDV), is a devastating disease in chickens characterized by the development of lymphomas throughout the body. Vaccine strains used against MD include gallid alphaherpesvirus 3 (GaAHV3), a non-oncogenic chicken alphaherpesvirus [...] Read more.
Marek’s disease (MD), caused by gallid alphaherpesvirus 2 (GaAHV2) or Marek’s disease herpesvirus (MDV), is a devastating disease in chickens characterized by the development of lymphomas throughout the body. Vaccine strains used against MD include gallid alphaherpesvirus 3 (GaAHV3), a non-oncogenic chicken alphaherpesvirus homologous to MDV, and homologous meleagrid alphaherpesvirus 1 (MeAHV1) or turkey herpesvirus (HVT). Previous work has shown most of the MDV gC produced during in vitro passage is secreted into the media of infected cells although the predicted protein contains a transmembrane domain. We formerly identified two alternatively spliced gC mRNAs that are secreted during MDV replication in vitro, termed gC104 and gC145 based on the size of the intron removed for each UL44 (gC) transcript. Since gC is conserved within the Alphaherpesvirinae subfamily, we hypothesized GaAHV3 (strain 301B/1) and HVT also secrete gC due to mRNA splicing. To address this, we collected media from 301B/1- and HVT-infected cell cultures and used Western blot analyses and determined that both 301B/1 and HVT produced secreted gC. Next, we extracted RNAs from 301B/1- and HVT-infected cell cultures and chicken feather follicle epithelial (FFE) skin cells. RT-PCR analyses confirmed one splicing variant for 301B/1 gC (gC104) and two variants for HVT gC (gC104 and gC145). Interestingly, the splicing between all three viruses was remarkably conserved. Further analysis of predicted and validated mRNA splicing donor, branch point (BP), and acceptor sites suggested single nucleotide polymorphisms (SNPs) within the 301B/1 UL44 transcript sequence resulted in no gC145 being produced. However, modification of the 301B/1 gC145 donor, BP, and acceptor sites to the MDV UL44 sequences did not result in gC145 mRNA splice variant, suggesting mRNA splicing is more complex than originally hypothesized. In all, our results show that mRNA splicing of avian herpesviruses is conserved and this information may be important in developing the next generation of MD vaccines or therapies to block transmission. Full article
(This article belongs to the Special Issue Marek's Disease Virus)
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