ArticleVeterinary research2025
Pathogenic and transcriptomic differences among porcine reproductive and respiratory syndrome viruses from distinct lineages in piglets.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Cross-Protection in PRRSV: Mechanisms, Limitations, and Implications for Vaccine Design.Pathogens (Basel, Switzerland) · 2026Review
- A Self-Assembling β-Annulus Nanoparticle Vaccine Incorporating OX40L Confers Partial Protection Against NADC30-Like PRRSV in Piglets.Transboundary and emerging diseases · 2026Article
- Longitudinal Molecular Epidemiology and Genomic Evolution of Porcine Reproductive and Respiratory Syndrome Virus in a Large-Scale Swine Production System in Northern China, 2023-2026.Transboundary and emerging diseases · 2026Article
- Genetic recombination and pathogenicity assessment of porcine reproductive and respiratory syndrome virus 2 strains in China.Frontiers in veterinary science · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is a highly recombinogenic pathogen that threatens global swine production. Multiple PRRSV lineages co-circulate in China, with lineage 1.8 being the predominant epidemic strain. However, the pathogenic characteristics and differences among strains from distinct lineages remain insufficiently studied. In this study, three novel recombinant PRRSV strains (GX-2428, GX-3264, and GX-5430) were isolated in Guangxi, China. Phylogenetic analysis of the ORF5 gene classified the three strains into lineage 3 (QYYZ-like), lineage 1.8 (NADC30-like), and lineage 1.5 (NADC34-like), respectively. Pathogenicity tests in piglets demonstrated that, compared with the control group, both GX-2428 and GX-3264 induced significant fever, whereas GX-5430 caused only a transient and milder febrile response. Infected piglets exhibited elevated levels of pro-inflammatory (IL-1β and TNF-α) and immunomodulatory cytokines (IL-4 and IL-10) compared to the control group. Postmortem analysis revealed that although viral shedding had ceased, high viral loads persisted in the lungs, tonsils, and lymph nodes of the infected piglets. Transcriptomic analysis of piglet lung tissues revealed that GX-5430 infection predominantly enriched pathways related to cellular transformation, signal transduction, and metabolic reprogramming. However, infections with GX-2428 or GX-3264 were significantly enriched in immune-related pathways, thereby inducing stronger immune activation and inflammatory responses. In conclusion, these findings highlight the recombination characteristics and lineage-specific pathogenic mechanisms of PRRSV, providing novel insights for the development of future prevention and control strategies.
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Registered trials
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