scholarly journals The Genomic and Pathogenic Characteristics of the Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Isolate WUH2

ISRN Virology ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Bin Li ◽  
Liurong Fang ◽  
Suyan Liu ◽  
Yunbo Jiang ◽  
Huanchun Chen ◽  
...  

To fully understand the extent of genetic diversity and pathogenesis of the highly pathogenic PRRSV found in China, we determined the genomic sequence of PRRSV WUH2; the pathogenicity of WUH2 was compared to the classical PRRSV isolate CH-1a. Our results showed that the WUH2 genome had a discontinuous deletion of 30 aa in Nsp2, a 1 nucleotide deletion located in both the 5′ and 3′ UTRs, and point mutations within GP5. Experimental infection demonstrated that PRRSV WUH2 reproduced the phenotype and symptoms of porcine high fever syndrome. Importantly, we found that there were differences in viral burden in the serum and tissues when comparing infections of the pathogenic isolate WUH2 to those of the classical isolate CH-1a. These data provide insight into the genomic diversity and altered pathogenicity of Chinese PRRSV isolates and help elucidate the evolution and potential pathogenic mechanisms of PRRSV.

2009 ◽  
Vol 83 (10) ◽  
pp. 5156-5167 ◽  
Author(s):  
Lei Zhou ◽  
Jialong Zhang ◽  
Jingwen Zeng ◽  
Shuoyan Yin ◽  
Yanhua Li ◽  
...  

ABSTRACT During the past 2 years, an atypical clinical outbreak, caused by a highly pathogenic porcine reproductive and respiratory syndrome virus (PRRSV) with a unique 30-amino-acid deletion in its Nsp2-coding region, was pandemic in China. In this study, we generated four full-length infectious cDNA clones: a clone of the highly virulent PRRSV strain JXwn06 (pWSK-JXwn), a clone of the low-virulence PRRSV strain HB-1/3.9 (pWSK-HB-1/3.9), a chimeric clone in which the Nsp2 region containing the 30-amino-acid deletion was replaced by the corresponding region of the low-virulence PRRSV strain HB-1/3.9 (pWSK-JXwn-HB1nsp2), and a mutated HB-1/3.9 clone with the same deletion in Nsp2 as JXwn06 (pWSK-HB1-ND30). We also investigated the pathogenicities of the rescued viruses (designated RvJXwn, RvJXwn-HB1nsp2, RvHB-1/3.9, and RvHB1-ND30, respectively) in specific-pathogen-free piglets in order to determine the role of the 30-amino-acid deletion in the virulence of the highly pathogenic PRRSV. All the rescued viruses could replicate stably in MARC-145 cells. Our findings indicated that RvJXwn-HB1nsp2 retained high virulence for piglets, like RvJXwn and the parental virus JXwn06, although the survival time of piglets infected with RvJXwn-HB1nsp2 was obviously prolonged. RvHB1-ND30 exhibited low virulence for piglets, like RvHB-1/3.9 and the parental virus HB-1/3.9. Therefore, we conclude that the 30-amino-acid deletion is not related to the virulence of the highly pathogenic PRRSV emerging in China.


2008 ◽  
Vol 89 (9) ◽  
pp. 2075-2079 ◽  
Author(s):  
Jian Lv ◽  
Jianwu Zhang ◽  
Zhi Sun ◽  
Weiquan Liu ◽  
Shishan Yuan

Since May 2006, a so-called ‘porcine high fever syndrome’ (PHFS) has spread all over China. The arterivirus porcine reproductive and respiratory syndrome virus (PRRSV) was believed to be the main causative agent, although the involvement of other pathogens was not formally excluded. The genome of a representative Chinese PRRSV strain, named JX143, was sequenced and used to develop infectious cDNA clones, pJX143 and pJX143M, with the latter containing an engineered MluI site that served as a genetic marker. In various virological assays, the rescued viruses, vJX143 and vJX143M, were indistinguishable from their parental virus. Animal experiments showed that these recombinant viruses retained the high pathogenicity and induced the typical clinical symptoms observed during PHFS outbreaks. This is the first report describing infectious cDNA clones of this highly pathogenic PRRSV. Our results unambiguously fulfil Koch's postulates and define highly pathogenic PRRSV as the aetiological agent of PHFS in China.


Virology ◽  
2013 ◽  
Vol 435 (2) ◽  
pp. 372-384 ◽  
Author(s):  
Baoqing Guo ◽  
Kelly M. Lager ◽  
Jamie N. Henningson ◽  
Laura C. Miller ◽  
Sarah N. Schlink ◽  
...  

2020 ◽  
Vol 94 (20) ◽  
Author(s):  
Guofei Ding ◽  
Jiaqi Liu ◽  
Qingyuan Shao ◽  
Bin Wang ◽  
Jian Feng ◽  
...  

ABSTRACT Claudins (CLDN) are a family of proteins that represent the most important components of tight junctions, where they establish the paracellular barrier that controls the flow of molecules in the intercellular space between epithelial cells. Several types of viruses make full use of CLDN to facilitate entry into cells. Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most important pathogens in the swine industry. In this study, we found that CLDN4 functions as an anti-PRRSV factor by blocking its absorption during the early stages of infection. The small extracellular loop (ECL2) of CLDN4 restricted the viral particles outside cells by binding to GP3. A novel function of GP3-mediated regulation of CLDN4 transcription was suggested. CLDN4 can be decreased through downregulating the level of CLDN4 transcription by ubiquitinating the transcription factor, SP1. The mechanism by which highly pathogenic PRRSV infects the epithelium was proposed. Importantly, ECL2 was found to block PRRSV absorption and infection and neutralize the virus. A more in-depth understanding of PRRSV infection is described, and novel therapeutic antiviral strategies are discussed. IMPORTANCE In the present study, the role of CLDN4 in PRRSV infection was studied. The results showed that CLDN4 blocked absorption into cells and restricted extracellular viral particles via the interaction between the CLDN4 small extracellular loop, ECL2, and the viral surface protein GP3. GP3 was found to downregulate CLDN4 through ubiquitination of the transcription factor SP1 to facilitate viral entry. The mechanism by which highly pathogenic PRRSV infects the epithelium is suggested. A novel function of GP3 in regulating gene transcription was discovered. Moreover, ECL2 could block PRRSV absorption and infection, as well as neutralizing the virus in the supernatant, which may lead to the development of novel therapeutic antiviral strategies.


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