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Recombinant characterization and pathogenicity of a novel L1C RFLP-1-4-4 variant of porcine reproductive and respiratory syndrome virus in China.
Vet Res
November 2024
State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150069, China.
Porcine reproductive and respiratory syndrome (PRRS) is one of the most significant diseases affecting the pig industry worldwide and is caused by the PRRS virus (PRRSV), which has complex genetic variation due to frequent mutations, indels, and recombination. The emergence of PRRSV L1C.5 in 2020 in the United States has raised worldwide concerns about PRRSV with the RFLP 1-4-4 pattern and lineage 1C.
View Article and Find Full Text PDFOccurrence of porcine reproductive and respiratory syndrome clinical outbreaks in Ontario sow herds, 2017 to 2019.
Can Vet J
November 2024
Department of Population Medicine, University of Guelph, 50 Stone Road East, Guelph, Ontario N1G 2W1 (Melmer, O'Sullivan, Greer, Friendship, Bonin Ferreira, Poljak); South West Ontario Veterinary Services, 500 Wright Blvd., Stratford, Ontario N4Z 1H3 (Moser); Department of Population Health and Pathology, North Carolina State University, 1060 William Moore Drive, Raleigh, North Carolina 27607, USA (Bonin Ferreira).
Background: Porcine reproductive and respiratory syndrome (PRRS) is one of the important endemic diseases in swine populations. Monitoring PRRS frequency in commercial herd populations has often been based on laboratory submissions. However, a limitation of this approach is that new clinical outbreaks of PRRS are challenging to identify if epidemiological information is not provided.
View Article and Find Full Text PDFPRRSV non-structural protein 5 inhibits antiviral innate immunity by degrading multiple proteins of RLR signaling pathway through FAM134B-mediated ER-phagy.
J Virol
October 2024
College of Veterinary Medicine, Northwest A&F University, Yangling, China.
Article Synopsis
- PRRSV employs non-structural protein 5 (Nsp5) to evade innate immune responses, particularly by inhibiting the expression of type I interferon (IFN-I) and interferon-stimulated genes (ISGs).
- The study reveals that Nsp5 degrades key proteins in the RIG-I-like receptor (RLR) signaling pathway, compromising the host's antiviral defenses.
- Additionally, Nsp5 promotes reticulophagy (ER-phagy) through interaction with FAM134B, facilitating the degradation of these RLR proteins and further aiding in viral persistence.
Whole-genome analysis of resilience based on the stability of reproduction performance during a porcine reproductive and respiratory syndrome virus outbreak in sows.
Animal
September 2024
Departament de Ciència Animal, Universitat de Lleida - AGROTECNIO-CERCA Centre, Av. Rovira Roure 191, 25198 Lleida, Spain. Electronic address:
Article Synopsis
- The Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) significantly impacts pig reproduction, causing issues like smaller litters and abortions in sows, with responses varying due to genetic differences.
- This study analyzed the reproductive performance of 183 sows to find 48 with extreme resilience to PRRSV, employing whole-genome sequencing to identify 16 genetic regions linked to their reproductive outcomes.
- Key genes identified are involved in viral entry and the immune response, suggesting potential genetic factors that influence a sow's ability to withstand PRRSV, but further validation with larger groups is needed.
Porcine γδ T cells express cytotoxic cell-associated markers and display killing activity but are not selectively cytotoxic against PRRSV- or swIAV-infected macrophages.
Front Immunol
August 2024
Vaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, SK, Canada.
Background: Gamma-delta (γδ) T cells are a major immune cell subset in pigs. Approximately 50% of circulating T cells are γδ T cells in young pigs and up to 30% in adult sows. Despite this abundance, the functions of porcine γδ T cells are mostly unidentified.
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