Sequence and phylogenetic analyses of Nsp2‐ HVII , ORF 5, and ORF 7 coding regions of highly pathogenic porcine reproductive and respiratory syndrome virus from Myanmar

2019 ◽  
Vol 66 (2) ◽  
pp. 1073-1076 ◽  
Author(s):  
Yamin Ko Ko ◽  
Perayot Pamonsinlapatham ◽  
Aung Myint ◽  
Aung Z. Latt ◽  
Kaythi Aye ◽  
...  
Keyword(s):  
Phylogenetic Analyses ◽  
Respiratory Syndrome Virus ◽  
Highly Pathogenic ◽  
Coding Regions ◽  
Orf 5

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

scholarly journals Identification the Presence of Clade 2.3.2.1c-Avian Influenza H5N1, a Highly Pathogenic Virus in Iraq, 2018

2019 ◽  
Vol 42 (2) ◽  
pp. 189-194
Author(s):  
Furkan Alaraji ◽  
Hussam Muhsen ◽  
Abdullah O. Alhatami ◽  
Yahia Ismail Khudhair
Keyword(s):  
Avian Influenza ◽  
Serological Test ◽  
Phylogenetic Analyses ◽  
Highly Pathogenic ◽  
Glycoprotein Gene ◽  
Pathogenic Virus ◽  
Hpai H5n1 ◽  
First Time ◽  
Clade 2.3.2.1C ◽  
Influenza H5n1

Abstract For the first time in Iraq, we identified in March, 2018 the presence of a highly virulent avian influenza virus (AIV), H5N1 (Clade 2.3.2.1c), causing highly pathogenic avian influenza (HPAI) in poultry farms, Iraq,. The identification of the virus was done using a rapid serological test, a real time-qPCR, and glycoprotein gene sequencing. Using sequencing and phylogenetic analyses, the clade 2.3.2.1c virus was recorded to be clustered, with high similarity to Asian and West African AIV, HPAI H5N1 from Ivory Coast identified in 2015. According to our knowledge, there was no previous detection of the clade 2.3.2.1c made in Iraq. Our results provide evidence that high risk of HPAI H5 outbreaks might be present in Iraq, and this needs to lead to high quality surveillance targeting of wild and domestic birds for early diagnosis of HPAI. The current work provides feasible and accurate approaches for understanding the evolution of HPAI H5 virus in different countries around the world.

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.

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