Widespread of NADC30-like PRRSV in China: Another Pandora's box for Chinese pig industry as the outbreak of highly pathogenic PRRSV in 2006?

Li, Xiangdong; Bao, Hongyan; Wang, Yang; Tian, Kegong

doi:10.1016/j.meegid.2016.12.021

Cited by 32 publications

(30 citation statements)

References 8 publications

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“…Bootstrap values were calculated using 1,000 replicates. The classifications of subgroups followed those described in previous studies (14)(15)(16)(17)26). To analyze the positions of the two consistently identified amino acid mutations in the spatial structure of NSP9, we predicted the three-dimensional structure of the protein using the I-TASSER online tool (http://zhanglab.ccmb.med.umich.edu/I-TASSER/), as previously described (24), as there is no direct structural information on any of the nidovirus RdRps (27).…”

Section: Cells Antibodies and Virusesmentioning

confidence: 99%

“…Highly pathogenic PRRSVs (HP-PRRSVs) likely originated from the Chinese subgroup 2 PRRSV and evolved through the intermediate subgroup 3 step by step (14). The newly emerged NADC30-like PRRSVs were defined as a new subgroup, as they share no more than 90% homology with the above-mentioned four subgroups and form a separate cluster in the phylogenetic tree (15)(16)(17)(18).…”

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confidence: 99%

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Two Residues in NSP9 Contribute to the Enhanced Replication and Pathogenicity of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus

Zhao

Gao

Xiong

et al. 2018

J Virol

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Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) possesses greater replicative capacity and pathogenicity than classical PRRSV. However, the factors that lead to enhanced replication and pathogenicity remain unclear. In our study, an alignment of all available full-length sequences of North American-type PRRSVs ( = 204) revealed two consistent amino acid mutations that differed between HP-PRRSV and classical PRRSV and were located at positions 519 and 544 in nonstructural protein 9. Next, a series of mutant viruses with either single or double amino acid replacements were generated from HP-PRRSV HuN4 and classical PRRSV CH-1a infectious cDNA clones. Deletion of either of the amino acids led to a complete loss of virus viability. In both Marc-145 and porcine alveolar macrophages, the replicative efficiencies of mutant viruses based on HuN4 were reduced compared to the parent, whereas the replication level of CH-1a-derived mutant viruses was increased. Plaque growth assays showed clear differences between mutant and parental viruses. In infected piglets, the pathogenicity of HuN4-derived mutant viruses, assessed through clinical symptoms, viral load in sera, histopathology examination, and thymus atrophy, was reduced. Our results indicate that the amino acids at positions 519 and 544 in NSP9 are involved in the replication efficiency of HP-PRRSV and contribute to enhanced pathogenicity. This study is the first to identify specific amino acids involved in PRRSV replication or pathogenicity. These findings will contribute to understanding the molecular mechanisms of PRRSV replication and pathogenicity, leading to better therapeutic and prognostic options to combat the virus. Porcine reproductive and respiratory syndrome (PRRS), caused by porcine reproductive and respiratory syndrome virus (PRRSV), is a significant threat to the global pig industry. Highly pathogenic PRRSV (HP-PRRSV) first emerged in China in 2006 and has subsequently spread across Asia, causing considerable damage to local economies. HP-PRRSV strains possess a greater replication capacity and higher pathogenicity than classical PRRSV strains, although the mechanisms that underlie these characteristics are unclear. In the present study, we identified two mutations in HP-PRRSV strains that distinguish them from classical PRRSV strains. Further experiments that swapped the two mutations in an HP-PRRSV strain and a classical PRRSV strain demonstrated that they are involved in the replication efficiency of the virus and its virulence. Our findings have important implications for understanding the molecular mechanisms of PRRSV replication and pathogenicity and also provide new avenues of research for the study of other viruses.

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Section: Cells Antibodies and Virusesmentioning

confidence: 99%

mentioning

confidence: 99%

Two Residues in NSP9 Contribute to the Enhanced Replication and Pathogenicity of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus

Zhao

Gao

Xiong

et al. 2018

J Virol

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“…In 2006, highly pathogenic PRRSV (HP‐PRRSV) emerged in China (An et al, ; Li et al, ; Tian et al, ; Tong et al, ). Since 2013, NADC30‐like PRRSV strains, which belong to NA‐type PRRSV with 131‐amino‐acid discontinuous deletions in NSP2 region, have been pandemic in China (Li, Bao, Wang, & Tian, ; Zhao et al, ; Zhou et al, ). Based on ORF5 sequences, NA‐type PRRSVs in China were now classified into five lineages: lineage 1, lineage 3, lineage 5, lineage 8 and lineage 9 (Gao et al, ).…”

Section: Introductionmentioning

confidence: 99%

Visual detection of porcine reproductive and respiratory syndrome virus using CRISPR‐Cas13a

Chang

Deng

et al. 2019

Transbound Emerg Dis

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Porcine reproductive and respiratory syndrome virus (PRRSV) has varied constantly and circulated in the pig industry worldwide. The prevention and control of porcine reproductive and respiratory syndrome (PRRS) is complicated. A visual, sensitive and specific diagnostic method is advantageous to the control of PRRS. The collateral cleavage activity of LwCas13a is activated to degrade non‐targeted RNA, when crRNA of LwCas13a bond to target RNA. The enhanced Cas13a detection is the combination of collateral cleavage activity of LwCas13a and recombinase polymerase amplification (RPA). In this study, the enhanced Cas13a detection for PRRSV was established. The novel method was an isothermal detection at 37°C, and the detection can be used for real‐time analysis or visual readout. The detection limit of the enhanced Cas13a detection was 172 copies/μl, and there were no cross‐reactions with porcine circovirus 2, porcine parvovirus, classical swine fever virus and pseudorabies virus. The enhanced Cas13a detection can work well in clinical samples. In summary, a visual, sensitive and specific nucleic acid detection method based on CRISPR‐Cas13a was developed for PRRSV.

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“…PRRSV was divided into two species: PRRSV‐1 (formerly European genotype 1) and PRRSV‐2 (formerly North American genotype 2) (Sinn et al., ). PRRSV NADC30 strain isolated from the United States in 2008 (Brockmeier et al., ) and from China in 2013 (Li, Bao, Wang, & Tian, ), which has three discontinuous deletions (a total of 131 amino acids) in nonstructural protein 2 (NSP2). In recent years, most studies confirmed that the outbreak of NADC30‐like strain have brought a great challenge to the prevention and control of major diseases in swine industry (Zhang et al., ; Zhou et al., ).…”

Section: Introductionmentioning

confidence: 99%

Porcine reproductive and respiratory syndrome virusNADC30‐like strain acceleratesStreptococcus suisserotype 2 infection in vivo and in vitro

Wang

Liu

et al. 2018

Transbound Emerg Dis

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Porcine reproductive and respiratory syndrome (PRRS), an economically significant pandemic disease, commonly results in increased impact of bacterial infections, including those by Streptococcus suis (S. suis). In recent years, PRRS virus (PRRSV) NADC30‐like strain has emerged in different regions of China, and coinfected with S. suis and PRRSV has also gradually increased in clinical performance. However, the mechanisms involved in host innate responses towards S. suis and their implications of coinfection with NADC30‐like strain remain unknown. Therefore, the pathogenicity of NADC30‐like strain and S. suis serotype 2 (SS2) coinfection in vivo and in vitro was investigated in this study. The results showed that NADC30‐like increased the invasion and proliferation of SS2 in blood and tissues, resulting in more severe pneumonia, myocarditis, and peritonitisas well as higher mortality rate in pigs. In vitro, NADC30‐like strain increased the invasion and survival of SS2 in porcine alveolar macrophages (PAM) cells, causing more drastic expression of inflammatory cytokines and activation of NF‐ĸB signalling. These results pave the way for understanding the interaction of S. suis with the swine immune system and their modulation in a viral coinfection.

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Widespread of NADC30-like PRRSV in China: Another Pandora's box for Chinese pig industry as the outbreak of highly pathogenic PRRSV in 2006?

Cited by 32 publications

References 8 publications

Two Residues in NSP9 Contribute to the Enhanced Replication and Pathogenicity of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus

Two Residues in NSP9 Contribute to the Enhanced Replication and Pathogenicity of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus

Visual detection of porcine reproductive and respiratory syndrome virus using CRISPR‐Cas13a

Porcine reproductive and respiratory syndrome virusNADC30‐like strain acceleratesStreptococcus suisserotype 2 infection in vivo and in vitro

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