A recombinant type 2 porcine reproductive and respiratory syndrome virus between NADC30-like and a MLV-like: Genetic characterization and pathogenicity for piglets

Porcine reproductive and respiratory syndrome virus (PRRSV) is an economically important pathogen for swine industryworldwide. The recombination occurring among PRRSV strains has been recognized as one of important molecularmechanisms for the evolution of PRRSV. Current prevalence of PRRSVNADC30-like causing clinical disease outbreaks is highly concerned in China. In the present study, the genetic characterization of a recombinant type 2 PRRSV (designated TJnh1501) was analyzed and its pathogenicity for piglets was examined. Our study showed that each region of TJnh1501 genome had 96.67-100% nucleotide and 96.5-100% amino acid identities with a Chinese highly pathogenic PRRSV-derivedmodified-live virus (MLV)-like except for its nonstructural protein 2 (nsp2)-coding region; while its nsp2-coding region shared higher nucleotide (84.44-85.85%) and amino acid (82.44-84.79%) identities with NADC30 and NADC30-like CHsx1401, and in particular, the highly variable region of nsp2 exhibited characteristic 131-aa deletion identical to NADC30 and NADC30-like CHsx1401. Meanwhile, we identified two recombination breakpoints located in the nt1737 and nt3506 of nsp2-coding region, which had higher nucleotide homologywith NADC30 andNADC30-like CHsx1401. Moreover, TJnh1501 infection could cause persistent fever, moderate respiratory clinical signs, higher viremia, and obvious gross and microscopic lung lesions in piglets. The virus was shown to have lower pathogenicity than HP-PRRSV JXwn06, but higher than NADC30-like CHsx1401 for piglets. Our findings reveal that TJnh1501 is a recombinant type 2 PRRSV from the recombinant event between NADC30-like and MLV-like derived from the Chinese highly pathogenic PRRSV, and it exhibits intermediate virulence for pigs. This study adds valuable evidence for understanding the role of genomic recombination in the evolution of PRRSV. (C) 2017 Elsevier B.V. All rights reserved.