Emergence of a novel highly pathogenic porcine reproductive and respiratory syndrome virus in China.
From 2014 to 2015, four novel highly pathogenic PRRS virus (HP-PRRSV) strains named 14 LY01-FJ, 14 LY02-FJ 15 LY01-FJ, and 15 LY02-FJ were isolated from high morbidity (100%) and mortality (40%-80%) in piglets and sows in Fujian Province. To further our knowledge about these novel virus strains, we characterized their complete genomes and determined their pathogenicity in piglets. Full-length genome sequencing analysis showed that these four isolates were closely related to type 2 (North American type, NA-type) isolates, with 88.1%-96.3% nucleotide similarity, but only 60.6%-60.8% homology to the Lelystad virus (LV) (European type, EU-type). The full length of the four isolates was determined to be 15017 or 15018 nucleotides (nt), excluding the poly(A) tail. Furthermore, the four isolates had three discontinuous deletions (aa 322-432, aa 483, and aa 504-522) within hypervariable region II (HV-II) of Nsp2, as compared to the reference strain VR-2332. This deletion pattern in the four isolates is consistent with strain MN184 and strain NADC30 isolated from America. Phylogenetic and molecular evolutionary analyses indicated that these virulent strains originated from a natural recombination event between the JXA1-like HP-PRRSV (JXA-1 is one of the earliest Chinese HP-PRRSV strains; sublineage 8.7) and the NADC30-like (lineage 1) PRRSV. Animal experiments demonstrated that these four strains caused significant weight loss and severe histopathological lung lesions as compared to the negative control group. High mortality rate (40% or 80%) was found in piglets infected with any one of the four strains, similar to that found with other Chinese HP-PRRSV strains. This study showed that the novel variant PRRSV was HP-PRRSV, and it is therefore critical to monitor PRRSV evolution in China and develop a method for controlling PRRS.