scholarly journals Determination of antibody induction by highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) vaccine: A comparison of two ELISA kits

2019 ◽  
Vol 81 (8) ◽  
pp. 1173-1176
Author(s):  
Meng GE ◽  
Run-Cheng LI ◽  
Wenjie GONG ◽  
Changchun TU
Keyword(s):  
Respiratory Syndrome Virus ◽  
Highly Pathogenic ◽  
Antibody Induction

scholarly journals Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0128292 ◽  
Author(s):  
Gang Wang ◽  
Ying Yu ◽  
Yabin Tu ◽  
Jie Tong ◽  
Yonggang Liu ◽  
...  
Keyword(s):  
Virus Infection ◽  
Respiratory Syndrome Virus ◽  
Highly Pathogenic ◽  
Induced Apoptosis

Immunogenicity of the highly pathogenic porcine reproductive and respiratory syndrome virus GP5 protein encoded by a synthetic ORF5 gene

Vaccine ◽  
2009 ◽  
Vol 27 (13) ◽  
pp. 1957-1963 ◽  
Author(s):  
Bin Li ◽  
Shaobo Xiao ◽  
Yanwei Wang ◽  
Shanshan Xu ◽  
Yunbo Jiang ◽  
...  
Keyword(s):  
Respiratory Syndrome Virus ◽  
Highly Pathogenic ◽  
Orf5 Gene

A novel HRM assay for differentiating classical strains and highly pathogenic strains of type 2 porcine reproductive and respiratory syndrome virus

2018 ◽  
Vol 39 ◽  
pp. 25-32 ◽  
Author(s):  
Junying Sun ◽  
Gali Bingga ◽  
Zhicheng Liu ◽  
Chunhong Zhang ◽  
Haiyan Shen ◽  
...  
Keyword(s):  
Respiratory Syndrome Virus ◽  
Highly Pathogenic

scholarly journals Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Induces Interleukin-17 Production via Activation of the IRAK1-PI3K-p38MAPK-C/EBPβ/CREB Pathways

2019 ◽  
Vol 93 (21) ◽  
Author(s):  
Honglei Wang ◽  
Li Du ◽  
Fang Liu ◽  
Zeyu Wei ◽  
Li Gao ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Molecular Mechanisms ◽  
Nonstructural Protein ◽  
Severe Pneumonia ◽  
Pi3k Inhibitor ◽  
Economic Losses ◽  
Respiratory Syndrome Virus ◽  
Binding Motif ◽  
Interleukin 17 ◽  
Highly Pathogenic

ABSTRACT Porcine reproductive and respiratory syndrome virus (PRRSV) is widely prevalent in pigs, resulting in significant economic losses worldwide. A compelling impact of PRRSV infection is severe pneumonia. In the present study, we found that interleukin-17 (IL-17) was upregulated by PRRSV infection. Subsequently, we demonstrated that PI3K and p38MAPK signaling pathways were essential for PRRSV-induced IL-17 production as addition of phosphatidylinositol 3-kinase (PI3K) and p38MAPK inhibitors dramatically reduced IL-17 production. Furthermore, we show here that deleting the C/EBPβ and CREB binding motif in porcine IL-17 promoter abrogated its activation and that knockdown of C/EBPβ and CREB remarkably impaired PRRSV-induced IL-17 production, suggesting that IL-17 expression was dependent on C/EBPβ and CREB. More specifically, we demonstrate that PRRSV nonstructural protein 11 (nsp11) induced IL-17 production, which was also dependent on PI3K-p38MAPK-C/EBPβ/CREB pathways. We then show that Ser74 and Phe76 amino acids were essential for nsp11 to induce IL-17 production and viral rescue. In addition, IRAK1 was required for nsp11 to activate PI3K and enhance IL-17 expression by interacting with each other. Importantly, we demonstrate that PI3K inhibitor significantly suppressed IL-17 production and lung inflammation caused by HP-PRRSV in vivo, implicating that higher IL-17 level induced by HP-PRRSV might be associated with severe lung inflammation. These findings provide new insights onto the molecular mechanisms of the PRRSV-induced IL-17 production and help us further understand the pathogenesis of PRRSV infection. IMPORTANCE Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) associated with severe pneumonia has been one of the most important viral pathogens in pigs. IL-17 is a proinflammatory cytokine that might be associated with the strong inflammation caused by PRRSV. Therefore, we sought to determine whether PRRSV infection affects IL-17 expression, and if so, determine this might partially explain the underlying mechanisms for the strong inflammation in HP-PRRSV-infected pigs, especially in lungs. Here, we show that PRRSV significantly induced IL-17 expression, and we subsequently dissected the molecular mechanisms about how PRRSV regulated IL-17 production. Furthermore, we show that Ser74 and Phe76 in nsp11 were indispensable for IL-17 production and viral replication. Importantly, we demonstrated that PI3K inhibitor impaired IL-17 production and alleviated lung inflammation caused by HP-PRRSV infection. Our findings will help us for a better understanding of PRRSV pathogenesis.

Upregulation of HMGB1 secretion in lungs of pigs infected by highly pathogenic porcine reproductive and respiratory syndrome virus

2021 ◽  
Vol 252 ◽  
pp. 108922
Author(s):  
Rong Wang ◽  
Yueqiang Xiao ◽  
Qian Zhang ◽  
Liang Bai ◽  
Weirong Wang ◽  
...  
Keyword(s):  
Respiratory Syndrome Virus ◽  
Highly Pathogenic
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