Reproductive Pathogenic Characteristics of a Highly Virulent Porcine Reproductive and Respiratory Syndrome Virus L1J (Lineage Korean Clade C) in Gilts

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) remains a major challenge to swine health and production globally. Among PRRSV-2 lineages circulating in South Korea, the lineage 1J (L1J)—recently reclassified from lineage Korean clade C (LKC)—has emerged as an epidemiologically significant variant, accounting for approximately 15%–28.9% of cases in recent years. Despite its widespread circulation, data on the reproductive pathogenicity of L1J strains remain scarce. To address this gap, an experimental infection study was conducted to evaluate the reproductive pathogenicity of PRRSV strain SNUVR220803 in pregnant gilts. This strain, originally classified within L1J and is characterized by multiple recombination events with lineage 5 viruses-presumably the Ingelvac PRRS MLV vaccine strain, as well as a unique four-amino acid deletion in Nsp2. Eight PRRSV-naïve pregnant gilts at 86 days of gestation were randomly assigned to either the infected (n = 4) or control (n = 4) group. Inoculated gilts exhibited elevated rectal temperatures at 2 days postinoculation (dpi), followed by clinical signs including anorexia and lethargy between 7 and 10 dpi. Clinical recovery was observed by 14 dpi; however, all infected gilts subsequently experienced abortion or premature farrowing at gestational days 109–112, during which no viable piglets were recovered, except for two that died within 30 min after birth without trauma, indicating intrauterine death or severe neonatal compromise. These findings demonstrate that SNUVR220803 possesses markedly higher reproductive pathogenicity than previously reported L1J strains, such as K07-2273. Given that PRRSV reproductive virulence cannot be fully explained by ORF5-based classification alone, the heightened pathogenicity of SNUVR220803 is likely attributed to a combination of mutations in nonstructural and structural proteins. These results highlight the need for continued molecular surveillance and pathogenicity studies of emerging PRRSV strains.