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Porcine Reproductive and Respiratory Syndrome / Viral Vaccines / Porcine Respiratory and Reproductive Syndrome Virus · Journal article
Virulence · August 26, 2026
A consensus or society position rather than new primary data.
This review articulates a unified mechanistic framework for PRRSV pathogenesis centered on regulated cell death (RCD) reprogramming and immune evasion, integrating molecular, cellular, and evolutionary evidence to inform precision vaccine design and diagnostic strategies. The authors argue that RCD-targeted interventions and consensus antigen design represent emerging strategies to overcome the challenge of rapid viral evolution, antigenic diversification, and immune dysfunction that underpin PRRSV persistence.
Narrative review article. Pigs infected with PRRSV in endemic regions; global swine production systems. Review synthesizes molecular, cellular, and evolutionary studies of viral pathogenesis and vaccine development.. Intervention: Emerging intervention strategies including consensus antigen design, rational attenuation, and nonreplicating platforms such as mRNA and protein nanoparticles; RCD-targeted therapeutic approaches.. Global; specific focus on Europe (PRRSV-1), North America, and Asia (PRRSV-2 and emerging lineage variants)..
Nsp5 directly targets STING to suppress the cGAS-STING-IFN antiviral axis, preventing STING trafficking and disabling host antiviral response NSP2 deletions show variable phenotypes: identical 30-amino-acid deletions produced strains with 60% mortality and nonpathogenic strains TJ-F19 strain carrying 120-amino-acid deletion in NSP2 shows reduced virulence and lower viral replication
NSP2 deletions show variable phenotypes: identical 30-amino-acid deletions produced strains with 60% mortality and nonpathogenic strains
Veterinary practitioners and swine production professionals should interpret this review as a framework for understanding why conventional vaccines have limited efficacy: PRRSV's capacity to reprogram cell death pathways and evade immunity, combined with rapid evolution, necessitates precision approaches targeting RCD pathways and consensus antigens rather than strain-specific designs. This understanding may guide selection of emerging vaccine platforms (mRNA, protein nanoparticles) and inform diagnostic strategies based on RCD biomarkers.
This is a comprehensive narrative review synthesizing molecular, cellular, and evolutionary evidence on PRRSV pathogenesis and vaccinology to frame a mechanistic understanding and strategic approach to intervention, without reporting original empirical data or clinical trials.
As stated by the source record.
Quoted from the source exactly as published.
Veterinary practitioners and swine production professionals should interpret this review as a framework for understanding why conventional vaccines have limited efficacy: PRRSV's capacity to reprogram cell death pathways and evade immunity, combined with rapid evolution, necessitates precision approaches targeting RCD pathways and consensus antigens rather than strain-specific designs. This understanding may guide selection of emerging vaccine platforms (mRNA, protein nanoparticles) and inform diagnostic strategies based on RCD biomarkers.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
PRRSV remains a major challenge because pathogenicity arises from the convergence of rapid viral evolution, immune evasion, and maladaptive host responses rather than from isolated virulence determinants. This review synthesizes evidence from molecular and cellular studies, arguing that recurrent recombination, lineage turnover, and antigenic diversification continuously reshape viral fitness, tissue tropism, and vaccine efficacy. PRRSV suppresses interferon‑driven antiviral programs while rewiring inflammatory signaling and intertwined lytic and non-lytic regulated cell death cascades. The virus induces a phenotypic convergence akin to PANoptosis, notably marked by hyper-inflammatory pyroptotic responses in macrophages, which in turn facilitates immune dysfunction, delays the development of protective immunity, and contributes to persistent infection. We assess emerging intervention strategies, including consensus antigen design, rational attenuation, and nonreplicating platforms such as mRNA and protein nanoparticles. This framework explores regulated cell death pathways as a basis for identifying diagnostic biomarkers and developing precision vaccines for PRRSV.
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