A single mutation in the PBC loop of VP2 is involved in the in vitro replication of infectious bursal disease virus  

作　　者：Xiaole Qi Xiang Gao Zhen Lu Lizhou Zhang Yongqiang Wang Li Gao Yulong Gao Kai Li Honglei Gao Changjun Liu Hongyu Cui Yanping Zhanga Xiaomei Wang 

机构地区：[1]Division of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, China [2]Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yangzhou 225009, China

出　　处：《Science China(Life Sciences)》2016年第7期717-723,共7页中国科学（生命科学英文版）

基　　金：supported by the National Natural Science Foundation of China (31430087);the Scientific and Technological Research Project of Harbin (2014AB3AN058);the Special Fund for Scientific and Technological Innovative Talents of Harbin (2014RFQYJ129);the Modern Agro-industry Technology Research System of China (nycytx-42-G3-01)

摘　　要：To test whether amino acid mutations in the PBC and PHI loops of VP2 are involved in the replication and virulence of infectious bursal disease virus(IBDV), a pair of viruses, namely the moderately virulent IBDV(rG x-F9VP2) and the attenuated strain(rGt), were used. Residue mutations A222P(P_(BC)) and S330R(PHI), selected by sequence comparison, were introduced individually into r Gx-F9VP2 by using a reverse genetics system. In addition, the reverse mutation of either P222 A or R330 S was introduced into r Gt. The four modified viruses were then rescued and evaluated in vitro(CEF cells) and in vivo(SPF chickens). Results showed that A222 P elevated the replication efficiency of rG x-F9VP2 while P222 A reduced that of rG t in CEF cells. A mutation at residue 330 did not alter IBDV replication. In addition, animal experiments showed that a single mutation at either residue 222 or 330 did not significantly influence the virulence of IBDV. In conclusion, residue 222 in PBC of VP2 is involved in the replication efficiency of IBDV in vitro but does not affect its virulence in vivo, further facilitating our understanding of the gene-function of IBDV.To test whether amino acid mutations in the PBc and PHI loops of VP2 are involved in the replication and virulence of infec- tious bursal disease virus （IBDV）, a pair of viruses, namely the moderately virulent IBDV （rGx-F9VP2） and the attenuated strain （rGt）, were used. Residue mutations A222P （PBc） and S330R （PHI）, selected by sequence comparison, were introduced individually into rGx-F9VP2 by using a reverse genetics system. In addition, the reverse mutation of either P222A or R330S was introduced into rGt. The four modified viruses were then rescued and evaluated in vitro （CEF cells） and in vivo （SPF chickens）. Results showed that A222P elevated the replication efficiency of rGx-F9VP2 while P222A reduced that of rGt in CEF cells. A mutation at residue 330 did not alter IBDV replication. In addition, animal experiments showed that a single mu- tation at either residue 222 or 330 did not significantly influence the virulence of IBDV. In conclusion, residue 222 in PBc of VP2 is involved in the replication efficiency of IBDV in vitro but does not affect its virulence in vivo, further facilitating our understanding of the gene-function of IBDV.

关 键 词：infectious bursal disease virus （IBDV） VP2 PUC REPLICATION 

分 类 号：S852.65[农业科学—基础兽医学]