Antigenic variants of pseudorabies virus (PRV) containing mutations in a viral glycoprotein with a molecular weight of 82,000 (gIII) were isolated by selecting for resistance to a complement-dependent neutralizing monoclonal antibody (MCA82-2) directed against gIII. These mutants were completely resistant to neutralization with MCA82-2 in the presence of complement. Two mutants selected for further studies either did not express gIII or expressed an improperly processed form of the glycoprotein. The mutations were also associated with an altered plaque morphology (syncytium formation). The gIII gene was mapped by marker rescue of a gIII- mutant with cloned restriction enzyme fragments to the long unique region of the PRV genome between 0.376 and 0.383 map units. This corresponds to the map location of a glycoprotein described by Robbins et al. (J. Mol. Appl. Gen. 2:485-496, 1984). Since gIII is nonessential for viral replication in cell culture and has several other characteristics in common with the herpes simplex virus glycoprotein gC, gIII may represent the PRV equivalent to herpes simplex virus gC.
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http://dx.doi.org/10.1128/JVI.58.1.173-178.1986 | DOI Listing |
Viruses
January 2025
State Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.
HDAC6 modulates viral infection through diverse mechanisms. Here, we investigated the role of HDAC6 in influencing viral infection in pig cells with the aim of exploiting the potential antiviral gene targets in pigs. Using gene knockout and overexpression strategies, we found that HDAC6 knockout greatly reduced PRV and VSV infectivity, whereas HDAC6 overexpression increased their infectivity in PK15 cells.
View Article and Find Full Text PDFAnimals (Basel)
January 2025
Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling 712100, China.
In 2020, severe diarrhea occurred in four-month-old fattening pigs from nine farms in Shandong Province, China. Fecal samples were collected from diseased pigs and tested by PCR for the presence of mammalian orthoreovirus (MRV), porcine epidemic diarrhea virus (PEDV), porcine deltacoronavirus (PDCoV), porcine rotavirus A (PoRVA), transmissible gastroenteritis virus (TGEV), porcine kobuvirus (PKV), and pseudorabies virus (PRV). The viral RNA of MRV and PEDV was detected in the fecal samples.
View Article and Find Full Text PDFJ Virol
January 2025
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Pseudorabies virus (PRV) is a porcine neurotropic alphaherpesvirus that infects peripheral tissues of its host, spreads into the nervous system, and establishes a life-long latency in neuronal cells. During productive infection, PRV replicates rapidly and causes pseudorabies or Aujeszky's disease. Reactivation from latent infection in the nervous system may lead to anterograde axonal transport of progeny virions, leading to recurrent infection of the epithelial layer and virus spread.
View Article and Find Full Text PDFVet Sci
January 2025
Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Diseases associated with porcine circovirus type 2 (PCV2) and pseudorabies virus (PRV) significantly affect the economy of pig farms, particularly when combined infections lead to bacterial co-infections. Antigens from the pseudorabies variant strain gB and gD proteins and PCV2 (genotyped) Cap protein were mixed with the pattern recognition receptor (PRR) agonist FLICd as adjuvants and formulated with a micro-hydrogel adjuvant into PCV2 and PRV bivalent subunit vaccines. Twenty pigs, aged 30-35 days, were divided into groups A (received bivalent subunit vaccine) and B (received bivalent subunit vaccines with recombinant FLICd adjuvant), as well as C (non-vaccinated challenge control) and D (blank control).
View Article and Find Full Text PDFPLoS Pathog
January 2025
Department of Translational Physiology, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
Gap junctions (GJs) play a pivotal role in intercellular communication between eukaryotic cells, including transfer of biomolecules that contribute to the innate and adaptive immune response. However, if and how viruses affect gap junction intercellular communication (GJIC) remains largely unexplored. Here, we describe how the alphaherpesvirus pseudorabies virus (PRV) triggers ERK1/2-mediated phosphorylation of the main gap junction component connexin 43 (Cx43) and closure of GJIC, which depends on the viral protein pUL46.
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