scholarly journals NADC30-Like Porcine Reproductive and Respiratory Syndrome in China

2017 ◽  
Vol 11 (1) ◽  
pp. 59-65 ◽  
Author(s):  
Kegong Tian

NADC30-like porcine reproductive and respiratory syndrome virus (PRRSV) has widely spread in China and become locally dominant virus strain in some provinces. Although they are not pathogenic as highly pathogenic PRRSV (HP-RRRSV) that outbreaks since 2006, NADC30-like PRRSVs distinguished themselves by high incidence of recombination with other virus strains which lead to change of virulence. The outbreaks of NADC30-like PRRSV in the vaccinated pig herds suggested that current commercial PRRSV vaccines cannot provide complete protection to the infection. In this review, we have described in detail the current situation of NADC30 PRRSV including epidemiology, genomic characterization, pathogenicity, and efficacy of current commercial vaccines in China.

Virology ◽  
2004 ◽  
Vol 321 (2) ◽  
pp. 383-390 ◽  
Author(s):  
T.V Grebennikova ◽  
D.F Clouser ◽  
A.C Vorwald ◽  
M.I Musienko ◽  
W.L Mengeling ◽  
...  

Vaccines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1020
Author(s):  
Yaozhong Ding ◽  
Ashenafi Kiros Wubshet ◽  
Xiaolong Ding ◽  
Zhongwang Zhang ◽  
Qian Li ◽  
...  

Vaccination is the best way to prevent economic losses from highly pathogenic porcine reproductive and respiratory syndrome virus (hp-PRRSV) disease. However, the commercially available vaccines need to periodically evaluate their efficacy against infections caused by new hp-PRRSV variants. Therefore, the objective of this study was to evaluate the efficacy of four (two modified live vaccines (MLV) and two inactivated) PRRSV commercial vaccines in piglets challenged with QH-08 and to estimate the genetic distance of the vaccine strains from recently isolated (QH-08) filed strain. Randomly, piglets (n = 5) allocated in groups 1–4 were immunized with Ingelvac PRRS MLV, CH-1a, JXA1, and JXA1-RMLV vaccines, whereas the infected and non-infected control piglets in groups 5 and 6 (n = 3), respectively, were subjected to PBS. Results indicated that JXA1 and JXA1-R MLV vaccines showed complete protection, but Ingelvac PRRS MLV and CH-1α vaccines revealed partial protection against the QH-08 PRRSV challenge. Similarly, vaccinated and challenged pigs showed lower macroscopic and microscopic lesions than the pigs in group 5. Our findings demonstrated a new insight that the variation in ORF1a and 1b coding sequence could significantly affect PRRSV vaccines efficacy. In conclusion, QH-08 is a good candidate for the design and development of an innovative PRRSV vaccine that ultimately helps in the control and prevention strategies.


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.


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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