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Two mutations in viral protein enhance the adaptation of waterfowl-origin H3N2 virus in murine model

文献类型: 外文期刊

作者: Yu, Zhijun 1 ; Cheng, Kaihui 4 ; Wang, Tiecheng 2 ; Ren, Zhiguang 5 ; Wu, Jiaqiang 1 ; He, Hongbin 3 ; Gao, Yuwei 2 ;

作者机构: 1.Shandong Acad Agr Sci, Inst Poultry Sci, 1 Jiaoxiao Rd, Jinan 250023, Shandong, Peoples R China

2.Acad Mil Med Sci, Mil Vet Res Inst, Key Lab Jilin Prov Zoonosis Prevent & Control, Changchun 130122, Jilin, Peoples R China

3.Shandong Normal Univ, Coll Life Sci, Jinan 250014, Shandong, Peoples R China

4.Shandong Acad Agr Sci, Dairy Cattle Res Ctr, Jinan 250132, Shandong, Peoples R China

5.Henan Univ, Sch Basic Med Sci, Joint Natl Lab Antibody Drug Engn, Kaifeng 475004, Peoples R China

关键词: H3N2; Avian influenza virus; Waterfowl; Mice; Pathogenesis

期刊名称:VIRUS RESEARCH ( 影响因子:3.303; 五年影响因子:3.445 )

ISSN: 0168-1702

年卷期: 2019 年 269 卷

页码:

收录情况: SCI

摘要: After serial passage of a waterfowl-origin H3N2 subtype avian influenza virus in BALB/c mice, we obtained H3N2 mouse-adapted variants and identified eight amino acid substitutions in five viral proteins in our previous study. Here, we analyze the key mutations determining viral pathogenicity in mammals. We found that both PB2-D701N mutation and M1-M192V mutation were implicated in the viral pathogenic phenotypic variation of H3N2 avian influenza virus in mice. Furthermore, we found that PB2-D701N could enhance viral replication in vitro and in vivo and expanded viral tissue tropism. Our data suggest that PB2-D701N and M1-M192V are the virulence markers of H3N2 avian influenza virus, and these markers can be used in the trans-species transmission surveillance for the H3N2 avian influenza virus.

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[1]Two mutations in viral protein enhance the adaptation of waterfowl-origin H3N2 virus in murine model. Yu, Zhijun,Wu, Jiaqiang,Wang, Tiecheng,Gao, Yuwei,He, Hongbin,Cheng, Kaihui,Ren, Zhiguang. 2019

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