广西1例人感染H9N2所致毒株的全基因组分子特征  

Genomic characteristics of a H9N2 avian influenza virus caused Human infection in Guangxi

作　　者：唐梅荣 蒋立立[2] 居昱[1] 陈敏玫[1,3] 莫建军 王晶[1,3] 曾竣[1] TANG Mei-rong;JIANG Li-li;JU Yu;CHEN Min-mei;MO Jian-jun;WANG Jing;ZENG Jun(Acute Infectious Disease Prevention and Control Institute,Guangxi Zhuang Autonomous Region Center for Disease Control and Prevention,Nanning,Guangxi 530028,China;Clinical Lab,Guilin Center for Disease Control and Prevention,Guilin,Guangxi 541000,China;Guangxi Key Laboratory of Major Infectious Disease Prevention and Control and Biosafety Emergency Response,Nanning,Guangxi 530028,China)

机构地区：[1]广西壮族自治区疾病预防控制中心急性传染病防制所,广西南宁530028 [2]桂林市疾病预防控制中心检验科,广西桂林541000 [3]广西重大传染病防控与生物安全应急响应重点实验室,广西南宁530028

出　　处：《热带医学杂志》2022年第11期1493-1497,1528,共6页Journal of Tropical Medicine

摘　　要：目的了解2018年10月桂林市确诊的1例人感染H9N2禽流感病毒的全基因组序列分子特征。方法对病例咽拭子标本分离毒株后进行全基因组测序,分析基因进化来源、致病性及毒力、宿主适应性、耐药位点以及糖基化位点等特征。结果该病例感染的H9N2毒株是HA基因裂解位点为RSSR↓G的低致病性禽流感病毒,属于H9.4.2.5分支,但存在炎症基序及多位点突变可致毒力增强。该禽流感病毒HA的受体结合位点为LMG,可致宿主偏好性改变,从易结合禽类受体α-2,3唾液酸改变成偏好结合人类受体α-2,6唾液酸,且HA蛋白存在D94N、S123P和T156A的突变,可增强病毒对人类受体的偏好结合。NA和PA基因未检测到神经氨酸酶类抑制剂和5’帽状结构(CAP)依赖型核酸内切酶抑制剂耐药突变,但M2基因存在对烷胺类药物耐药的S31N突变。HA蛋白存在8个潜在糖基化位点,未发生糖基化位点数目增减突变,但丢失218位点,新增313位点的糖基化。结论广西的H9N2禽流感病毒经过重组变异已获得了感染并适应人类宿主的能力,为防止H9N2亚型或重组新型禽流感在人间大流行,须加强其分子进化方面的监测。Objective To analyze the whole genetic characteristics of a H9N2 avian influenza virus in one infected humancase in Guilin in October 2018.MethodsGenome-wide sequencing was performed on the strain isolated from pharyngealswab sample to analyze the characteristics of gene origin,pathogenicity and virulence,host adaptability,drug resistancesites and glycosylation sites of an avian influenza virus.ResultsThe H9N2 strain in this infected human case was a lowpathogenic avian influenza virus with the cleavage site of HA gene RSSR↓G,belonging to the H9.4.2.5 branch,but withinflammatory motifs and multiple site mutations resulting in the invirulence.The receptor binding site of HA of this avianinfluenza virus was LMG,which could change the host preference from the bird receptorα-2,3 sialic acid to the humanreceptorα-2,6 sialic acid receptor.Moreover,there were D94N,S123P and T156A mutations in HA protein,which couldenhance the virus preference for human receptor binding.There was no neuraminidase inhibitor and 5’CAP dependentendonuclease inhibitor resistance mutation in NA and PA genes,but the M2 gene had a S31N mutation contributing toresistant to alkamines.There were 8 potential glycosylation sites in HA protein with no mutation in totality,but the 218 sitewas lost and the 313 site added.ConclusionsH9N2 avian influenza viruses in Guangxi had acquired the ability to infectand adapt to human hosts through recombination and mutation.The monitoring of molecular evolution of H9N2 subtype avianinfluenza viruses should be strengthened.

关 键 词：禽流感病毒 H9N2 人感染病例 分子特征 

分 类 号：R511.7[医药卫生—内科学]