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Articles by Peirong Jiao
Total Records ( 3 ) for Peirong Jiao
  Hailiang Sun , Peirong Jiao , Yuqiang Cheng , Runyu Yuan , Pengfei Cui , Liming Jin , Chaoan Xin and Ming Liao
  H5N1 Highly Pathogenic Avian Influenza (HPAI) viruses have posed a serious threat to poultry, wild birds and mammals including humans since 1997. Quails are a potential reservoir in which influenza viruses might mutate to a mammalian transmissible form. To investigate the molecular changes that occur in H5N1 HPAI viruses following passage in quail, two isolates, A/Quail/Guangdong/342/2008 (QL342) and A/Qquail/Guangdong/176/2004 (QL176) were selected. QL342 (clade 2.3.2) and QL176 (clade 7) viruses were high pathogenic to quail with a mortality rate of 18.3-100% and could be transmitted between naive contact quails. After six passages in Japanese quails, researchers obtained two viruses, F6QL342 and F6QL176. Compared with QL342, F6QL342 had six animo acid substitutions in polymerases PB1 and PA, Nucleoprotein (NP) and Hemagglutinin (HA) but there was little difference in their pathogenicity to mice. Compared with QL176, F6QL176 virus had 10 amino acid substitutions in PB2, NA, HA proteins. F6QL176 showed an increased pathogenicity towards mice causing more severe weight loss and higher lethality compared with QL176. The findings showed that quails might play an important role in the adaptation of H5N1 avian influenza viruses to mammals. Therefore, researchers should enhance surveillance of H5N1 HPAI viruses in the quail population especially in live-bird markets.
  Peirong Jiao , Guobin Tian , Yanbing Li , Guohua Deng , Yongping Jiang , Chang Liu , Weilong Liu , Zhigao Bu , Yoshihiro Kawaoka and Hualan Chen
  In this study, we explored the molecular basis determining the virulence of H5N1 avian influenza viruses in mammalian hosts by comparing two viruses, A/Duck/Guangxi/12/03 (DK/12) and A/Duck/Guangxi/27/03 (DK/27), which are genetically similar but differ in their pathogenicities in mice. To assess the genetic basis for this difference in virulence, we used reverse genetics to generate a series of reassortants and mutants of these two viruses. We found that a single-amino-acid substitution of serine for proline at position 42 (P42S) in the NS1 protein dramatically increased the virulence of the DK/12 virus in mice, whereas the substitution of proline for serine at the same position (S42P) completely attenuated the DK/27 virus. We further demonstrated that the amino acid S42 of NS1 is critical for the H5N1 influenza virus to antagonize host cell interferon induction and for the NS1 protein to prevent the double-stranded RNA-mediated activation of the NF-ĸB pathway and the IRF-3 pathway. Our results indicate that the NS1 protein is critical for the pathogenicity of H5N1 influenza viruses in mammalian hosts and that the amino acid S42 of NS1 plays a key role in undermining the antiviral immune response of the host cell.
  Qiyun Zhu , Huanliang Yang , Weiye Chen , Wenyan Cao , Gongxun Zhong , Peirong Jiao , Guohua Deng , Kangzhen Yu , Chinglai Yang , Zhigao Bu , Yoshihiro Kawaoka and Hualan Chen
  In 2001 and 2003, we isolated two H5N1 viruses, A/swine/Fujian/1/01 (SW/FJ/01) and A/swine/Fujian/1/03 (SW/FJ/03), from pigs in Fujian Province, southern China. Genetically, these two viruses are similar, although the NS gene of the SW/FJ/03 virus has a 15-nucleotide deletion at coding positions 612 to 626. The SW/FJ/01 virus is highly lethal for chickens, whereas the SW/FJ/03 virus is nonpathogenic for chickens when administrated intravenously or intranasally. To understand the molecular basis for the difference in virulence, we used reverse genetics to create a series of single-gene recombinants of both viruses. We found that a recombinant virus containing the mutated NS gene from the SW/FJ/03 virus in the SW/FJ/01 virus background was completely attenuated in chickens. We also found that viruses expressing the mutant NS1 protein of SW/FJ/03 did not antagonize the induction of interferon (IFN) protein. Conversely, only the recombinant virus containing the wild-type SW/FJ/01 NS gene in the SW/FJ/03 background was lethal in chickens and antagonized IFN protein levels. Further, we proved that the NS1 genes of the two viruses differ in their stabilities in the host cells and in their abilities to interact with the chicken cleavage and polyadenylation specificity factor. These results indicate that the deletion of amino acids 191 to 195 of the NS1 protein is critical for the attenuation of the SW/FJ/03 virus in chickens and that this deletion affects the ability of the virus to antagonize IFN induction in host cells.
 
 
 
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