Biological properties of a duck enteritis virus attenuated via serial passaging in chick embryo fibroblasts

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• 作者：Chenghuai Yang (1)
  Junping Li (1)
  Qihong Li (1)
  Ling Li (1)
  Miao Sun (1)
  Huijiao Li (1)
  Yecai Xia (1)
  Hanchun Yang (2)
  Kangzhen Yu (3)
  
  1. China Institute of Veterinary Drug Control ; No. 8 Zhongguancun South Street ; Haidian District ; Beijing ; 100081 ; People鈥檚 Republic of China
  2. Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture ; College of Veterinary Medicine and State Key Laboratory of Agrobiotechnology ; China Agricultural University ; No. 2 Yuanmingyuan West Road ; Haidian District ; Beijing ; 100193 ; People鈥檚 Republic of China
  3. Ministry of Agriculture ; No. 11 Nongzhanguan Nanli ; Chaoyang District ; Beijing ; 100125 ; People鈥檚 Republic of China
  
• 刊名：Archives of Virology
• 出版年：2015
• 出版时间：January 2015
• 年：2015
• 卷：160
• 期：1
• 页码：267-274
• 全文大小：1,883 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Virology
  Medical Microbiology
  Infectious Diseases
  
• 出版者：Springer Wien
• ISSN：1432-8798

文摘

To gain a better understanding of the genetic changes required for attenuation of duck enteritis virus (DEV), the Chinese standard challenge strain of DEV (DEV CSC) was serially passaged 80 times in chick embryo fibroblasts. We plaque-purified the virus after the 25th passage (DEV p25) and the 80th passage (DEV p80) and investigated its in vitro and in vivo properties. Average plaque sizes for DEV p25 and p80 were significantly smaller than those for their parental DEV CSC. The results from an in vivo experiment revealed that DEV p25 and p80 were avirulent in ducks and protected them from virulent DEV challenge. The complete genome sequence of DEV p80 was determined and compared with that of the parent virus. An 1801-bp deletion was identified in the genome of DEV p80, which affected the genes encoding gI and gE. Moreover, there were 11 base substitutions, which led to seven amino acid changes in open reading frames LORF9, UL51, UL9, UL7, UL4, ICP4 and US3. Further DNA sequence analysis showed that the 1801-bp deletion was also present in DEV p25. Our findings suggest that DEV gE and/or gI are nonessential for virus growth and might, as with other herpesviruses, play an important role in cell-to-cell spread and virulence. Our experiments provide more genetic information about DEV attenuation and further advance our understanding of the molecular basis of DEV pathogenesis.