Pathogenesis, Immunology and Epidemiology of Veterinary Viruses—2nd Edition

A special issue of Animals (ISSN 2076-2615). This special issue belongs to the section "Veterinary Clinical Studies".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 656

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Guest Editor
State Key Laboratory for Animal Disease Control and Prevention, National Foot and Mouth Diseases Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China
Interests: foot-and-mouth disease virus; African swine fever virus; Seneca Valley virus; innate immune response; metabolism; pathogenesis; interaction
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Special Issue Information

Dear Colleagues,

Veterinary viruses seriously harm the health of livestock, domestic animals and wildlife. Studies of these viruses mainly include virus-induced pathogenesis, immunity and epidemiology. As we know, almost two-thirds of the pathogens that cause diseases in humans (SARS-CoV-2, avian influenza virus, Ebola virus, etc.) are of animal origin. In addition to these zoonoses, some animal-species-specific viruses, such as African swine fever virus (ASFV), classical swine fever virus (CSFV), foot-and-mouth disease virus (FMDV), etc., are also extremely important. The aim of this Special Issue is to publish original research papers or reviews concerning the pathogenesis, immunology and epidemiology of viruses in pigs or chickens.

Research areas include the following: findings on pathogenesis and epidemiology, both innate and adaptive immune responses, the immune escape of viruses; and virus–host interactions.

We invite you to share your recent findings through this Special Issue. We look forward to receiving your contributions.

Dr. Huisheng Liu
Guest Editor

Manuscript Submission Information

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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. Animals is an international peer-reviewed open access semimonthly 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 2400 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

  • animals
  • veterinary viruses
  • pathogenesis
  • epidemiology
  • innate immune response
  • adaptive immune response
  • cross-species infection
  • interaction

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Published Papers (1 paper)

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Research

13 pages, 1357 KB  
Article
ELAVL1 Promotes Proliferation and Inhibits Apoptosis of the Marek’s Disease Virus (MDV)-Transformed Cell Line MSB1 via the COX-2/PGE2 Pathway
by Lei He, Dong-Mei Zhan, Hui Peng, Meng-Ru Gao, Jian Chen, Yan-Yan Jia, Cheng-Shui Liao, Song-Biao Chen, Ke Ding and Zu-Hua Yu
Animals 2026, 16(5), 843; https://doi.org/10.3390/ani16050843 - 7 Mar 2026
Viewed by 469
Abstract
Marek’s disease (MD), caused by the oncogenic Marek’s disease virus (MDV), is a highly contagious avian infection that induces lymphoproliferative tumors. The RNA-binding protein ELAVL1 is known to regulate tumor cell proliferation and apoptosis, but its role in MDV-induced oncogenesis remains unclear. This [...] Read more.
Marek’s disease (MD), caused by the oncogenic Marek’s disease virus (MDV), is a highly contagious avian infection that induces lymphoproliferative tumors. The RNA-binding protein ELAVL1 is known to regulate tumor cell proliferation and apoptosis, but its role in MDV-induced oncogenesis remains unclear. This study investigated whether ELAVL1 modulates proliferation and apoptosis in the MDV-transformed MSB1 cell line and whether its effects involve the cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) pathway. MSB1 cells were transiently transfected with ELAVL1-overexpressing plasmids (pEGFP-C-ELAVL1) or ELAVL1-specific siRNA, with expression confirmed by real-time PCR (qRT-PCR). Cell proliferation was assessed using the CCK-8 assay, while cell cycle distribution and apoptosis rates were analyzed by flow cytometry. COX-2 and PGE2 expression levels were determined by qRT-PCR, Western blotting, and ELISA. Overexpression of ELAVL1 significantly promoted the proliferation of MSB1 cells, decreased transition into the G1 phase, increased the proportions of S and G2 phase cells, and suppressed apoptosis. Correspondingly, both mRNA and protein levels of COX-2 and PGE2 were significantly elevated. Conversely, ELAVL1 knockdown significantly inhibited proliferation, induced G1 phase arrest, decreased S phase cells, and significantly decreased COX-2 and PGE2 expression. These findings indicate that ELAVL1 promotes proliferation and inhibits apoptosis in MDV-transformed MSB1 cells, potentially via the COX-2/PGE2 signaling pathway. Full article
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