Abstract
Highly pathogenic porcine reproductive and respiratory syndrome (HP-PRRS) emerged in China in 2006, and HP-PRRS virus (HP-PRRSV) has evolved continuously. Here, the complete genomic sequence of a novel HP-PRRSV field strain, JX, is reported. The present finding will contribute to further studies focusing on the evolutionary mechanism of PRRSV.
GENOME ANNOUNCEMENT
In May 2006, highly pathogenic porcine reproductive and respiratory syndrome (HP-PRRS) attacked the swine industry of China, with the characteristics of high fever and high morbidity and mortality in pigs of all ages. The causative agent was the HP-PRRS virus (HP-PRRSV), which was observed to have a unique molecular hallmark, namely, a discontinuous deletion of 30 amino acids in nonstructural protein 2 (Nsp2); it belongs to the North American genotype (type II) (1, 5, 7, 9). In the past 6 years, HP-PRRS has reemerged several times and has resulted in immense economic losses for the China swine industry (10). PRRSV evolves rapidly, and its evolutionary rate is the highest among RNA viruses reported so far (3). Homologous recombination between circulating viruses also accelerates PRRSV evolution (2, 4, 6).
Here, a field HP-PRRSV strain, JX, was isolated from lymph nodes of a 4-month-old pig with respiratory symptoms in south China in 2010. Pigs on this farm had a high death rate of nearly 86%. Twelve pairs of primers were designed, based on the consensus region of HP-PRRSV sequences deposited in GenBank. The PCR products were cloned into a pMD18-T vector (TaKaRa) and sequenced. The terminal sequences were determined using a kit for rapid amplification of cDNA ends (RACE; Clontech). Then, the sequence data were assembled into one contiguous sequence of 15,320 nucleotides, excluding the poly(A) tail. Sequence alignment was performed using Clustal X 2.1, and a phylogenetic tree was constructed using MEGA 5.
The phylogenetic tree showed that JX belongs to the 2009 to 2010 HP-PRRSV isolate subgroup, which is genetically different from the 2006 to 2008 HP-PRRSV isolates subgroup (8, 10). Novel amino acid changes were found within both nonstructual proteins and structural proteins: one within Nsp2, one within Nsp4, one within Nsp7β, one in Nsp12, and one in glycoprotein 4 (GP4). Moreover, three amino acids within Nsp2 are different from other HP-PRRSV strains but are identical to conventional PRRSV strains. Besides, one nucleotide within Nsp2, one nucleotide within Nsp9, two nucleotides within Nsp10, two nucleotides within Nsp11, one nucleotide within Nsp12, and one nucleotide within ORF2a were different from other HP-PRRSV strains but are identical with conventional PRRSV strains, although there was no resulting amino acid change.
The evolutionary mechanism underlying the difference between JX and other HP-PRRSV strains cannot yet be precisely explained. We speculate that JX might be the uncovered evolutionary intermediate form. The present finding indicates that HP-PRRSV continues to evolve in China and will contribute to further studies focusing on the evolutionary mechanism of PRRSV. The results also enhance the importance of rational design of vaccines with broad-spectrum protective capabilities.
Nucleotide sequence accession number.
The complete genomic sequence of HP-PRRSV strain JX was deposited in GenBank under accession no. JX317649.
ACKNOWLEDGMENTS
This work was supported by a Faculty Starting Grant and the State Key Laboratory of Agrobiotechnology (grant 2010SKLAB06-1), China Agricultural University, China.
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