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Nsp9 and Nsp10 Contribute to the Fatal Virulence of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Emerging in China


PRRS is a considerable threat to the pig industry worldwide. A large-scale atypical PRRS caused by highly pathogenic PRRSV (HP-PRRSV) that emerged in 2006 has resulted in considerable economic loss to Chinese pig production. The disease is characterized by a high body temperature (41°C–42°C), morbidity and by mortality of the affected pigs. Although the genomic marker, the 30-amino-acid deletion in its Nsp2-coding region has been previously verified to have no relation to its increased pathogenicity, the genomic region(s) associated with the fatal virulence of HP-PRRSV remain unclear. A series of chimeric viruses with swapped coding regions between HP- and LP-PRRSV were constructed, and their growth abilities and pathogenicities in piglets were analyzed. Our results demonstrated that Nsp9 and Nsp10 together contribute to the replication efficiency and the fatal virulence of HP-PRRSV for piglets. Our finding is not only the first unambiguous illumination concerning the key virulence determinant of Chinese HP-PRRSV but it also provides a novel insight for understanding the molecular pathogenesis of this virus and for designing new drugs and vaccines against PRRSV infection in the future.


Vyšlo v časopise: Nsp9 and Nsp10 Contribute to the Fatal Virulence of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Emerging in China. PLoS Pathog 10(7): e32767. doi:10.1371/journal.ppat.1004216
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004216

Souhrn

PRRS is a considerable threat to the pig industry worldwide. A large-scale atypical PRRS caused by highly pathogenic PRRSV (HP-PRRSV) that emerged in 2006 has resulted in considerable economic loss to Chinese pig production. The disease is characterized by a high body temperature (41°C–42°C), morbidity and by mortality of the affected pigs. Although the genomic marker, the 30-amino-acid deletion in its Nsp2-coding region has been previously verified to have no relation to its increased pathogenicity, the genomic region(s) associated with the fatal virulence of HP-PRRSV remain unclear. A series of chimeric viruses with swapped coding regions between HP- and LP-PRRSV were constructed, and their growth abilities and pathogenicities in piglets were analyzed. Our results demonstrated that Nsp9 and Nsp10 together contribute to the replication efficiency and the fatal virulence of HP-PRRSV for piglets. Our finding is not only the first unambiguous illumination concerning the key virulence determinant of Chinese HP-PRRSV but it also provides a novel insight for understanding the molecular pathogenesis of this virus and for designing new drugs and vaccines against PRRSV infection in the future.


Zdroje

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