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当前位置: 首页 > 文章 > H3N2犬流感病毒PB2 E~(627)K突变对小鼠致病性的影响 中国预防兽医学报 2017,39 (5) 346-350+355
Position: Home > Articles > Effect of PB2 E~(627)K on the pathogenicity of H3N2 canine influenza virus in mice Chinese Journal of Preventive Veterinary Medicine 2017,39 (5) 346-350+355

H3N2犬流感病毒PB2 E~(627)K突变对小鼠致病性的影响

作  者：
黄三;曾伟杰;张欣;郑运;王丽芳;周沛;李守军
单  位：
广东省兽医临床重大疾病综合防控重点实验室;广东省宠物工程技术研究中心;华南农业大学兽医学院
关键词：
犬流感;反向遗传;定点突变;E627K
摘  要：
甲型流感病毒PB2蛋白627位点突变(E~(627)K)是影响流感病毒宿主适应性和致病性的重要因素之一。本实验室前期研究分离的H3N2亚型犬流感病毒(CIV)GD02株(A/canine/Guangdong/02/2011)PB2蛋白序列的627位点氨基酸为谷氨酸,为研究该病毒株PB2的E~(627)K突变对小鼠致病性的影响,本实验采用反向遗传操作技术获得rGD02,并利用定点突变技术拯救了PB2 627位点发生突变的rGD02-E~(627)K。通过接种小鼠比较rGD02和rGD02-E~(627)K对小鼠致病性的差异,评价PB2 E~(627)K突变对H3N2 CIV致病性的影响。结果显示,rGD02和rGD02-E~(627)K对小鼠均无致死性(MLD50>106EID50),对小鼠增重的影响差异均不显著,而且这两株病毒对小鼠的致病性也无明显差异。表明PB2 E~(627)K并未显著影响H3N2 CIV对小鼠的致病性,该研究建立的H3N2 CIV反向遗传操作平台和定点突变技术为该病毒后续的致病机理、基因功能研究及疫苗研制奠定了基础。
译  名：
Effect of PB2 E~(627)K on the pathogenicity of H3N2 canine influenza virus in mice
作  者：
HUANG San;ZENG Wei-jie;ZHANG Xin;ZHENG Yun;WANG Li-fang;ZHOU Pei;LI Shou-jun;College of Veterinary Medicine, South China Agricultural University;Guangdong Provincial Key Laboratory of Prevention and Control for Severe Clinical Animal Diseases;Guangdong Technological Engineering Research Center for Pet;
关键词：
canine influenza;;reserve genetic system;;site directed mutagenesis;;E~(627)K
摘  要：
Substitution of lysine at 627 position in PB2 protein(E~(627)K) has been recognized as a determinant for host adaptation and virulent element for influenza A viruses. The H3N2 subtype canine influenza virus(CIV) of A/canine/Guangdong/02/2011(GD02) isolated by this Lab possessed a glutamic acid(627E) in PB2. To explore the potential role of E~(627) K substitution in PB2 in the H3N2 CIV, we compared the biology properties and pathogenicity in mice between the rescued virus rGD02 containing 627 E in PB2 and the mutation virus rGD02-E~(627) K containing 627 K. The rGD02 and rGD02-E~(627) K were rescued by the GD02 reverse genetic system and site-directed mutation technology. Then, rGD02 and rGD02-E~(627) K pathogenicity were tested in mice to evaluate the PB2 E~(627) K mutation influence of H3N2 CIV on the pathogenicity. The results showed that both rGD02 and rGD02-E~(627) K were not fatal to mice(MLD50>106 EID50) and had limited effects on mice body weight, indicating that the pathogenicity of rGD02 and rGD02-E~(627) K to mice were no significant difference. The studies suggested a 627 K substitution in PB2 had on impact on the pathogenic for the H3N2 CIV to mice.

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