国际病毒学杂志
國際病毒學雜誌
국제병독학잡지
INTERNATIONAL JOURNAL OF VIROLOGY
2015年
1期
4-10
,共7页
靳淼%张翠红%李慧莹%何雅青%孔翔羽%章青%封少龙%段招军
靳淼%張翠紅%李慧瑩%何雅青%孔翔羽%章青%封少龍%段招軍
근묘%장취홍%리혜형%하아청%공상우%장청%봉소룡%단초군
诺如病毒%急性胃肠炎%GⅡ.4基因型%变异株%人组织血型抗原
諾如病毒%急性胃腸炎%GⅡ.4基因型%變異株%人組織血型抗原
낙여병독%급성위장염%GⅡ.4기인형%변이주%인조직혈형항원
Norovirus%Acute gastroenteritis%GⅡ.4 genotype%Variants%Human histo-blood group antigen
目的 了解GⅡ.4型诺如病毒不同变异株与受体人组织血型抗原(human histo-blood group antigens,HBGAs)的结合模式及HBGAs在GⅡ.4型诺如病毒进化过程中的角色.方法 利用RT-PCR方法扩增5株不同GⅡ.4型诺如病毒变异株的衣壳蛋白P区序列,在原核系统中表达并纯化P蛋白.通过一组HBGAs表型明确的唾液样本与P蛋白结合,进行唾液HBGAs结合模式分析.同时,将P蛋白与人工合成的HBGAs寡糖进行寡糖结合分析.结果 唾液HBGAs结合模式分析表明,Sakai变异株几乎不结合,其他GⅡ.4变异株的HBGAs结合模式相似,与分泌型唾液(A、B、AB和O型分泌型)结合,与O型非分泌型唾液不结合.95/96US变异株和2006b变异株结合能力较高,其次是Camberwell变异株,Hunter变异株较弱.寡糖结合分析与唾液结合分析结果一致,Sakai变异株不结合,其他毒株与均与分泌型寡糖(Ley和H1)结合,与非分泌型寡糖(Lea和Lex)不结合.95/96US变异株和2006b变异株与寡糖的结合能力较强,其次是Camberwell变异株.结论 绝大多数GⅡ.4型诺如病毒变异株与HBGAs结合模式相同,但结合能力不同,结合能力强的变异株流行范围较广.
目的 瞭解GⅡ.4型諾如病毒不同變異株與受體人組織血型抗原(human histo-blood group antigens,HBGAs)的結閤模式及HBGAs在GⅡ.4型諾如病毒進化過程中的角色.方法 利用RT-PCR方法擴增5株不同GⅡ.4型諾如病毒變異株的衣殼蛋白P區序列,在原覈繫統中錶達併純化P蛋白.通過一組HBGAs錶型明確的唾液樣本與P蛋白結閤,進行唾液HBGAs結閤模式分析.同時,將P蛋白與人工閤成的HBGAs寡糖進行寡糖結閤分析.結果 唾液HBGAs結閤模式分析錶明,Sakai變異株幾乎不結閤,其他GⅡ.4變異株的HBGAs結閤模式相似,與分泌型唾液(A、B、AB和O型分泌型)結閤,與O型非分泌型唾液不結閤.95/96US變異株和2006b變異株結閤能力較高,其次是Camberwell變異株,Hunter變異株較弱.寡糖結閤分析與唾液結閤分析結果一緻,Sakai變異株不結閤,其他毒株與均與分泌型寡糖(Ley和H1)結閤,與非分泌型寡糖(Lea和Lex)不結閤.95/96US變異株和2006b變異株與寡糖的結閤能力較彊,其次是Camberwell變異株.結論 絕大多數GⅡ.4型諾如病毒變異株與HBGAs結閤模式相同,但結閤能力不同,結閤能力彊的變異株流行範圍較廣.
목적 료해GⅡ.4형낙여병독불동변이주여수체인조직혈형항원(human histo-blood group antigens,HBGAs)적결합모식급HBGAs재GⅡ.4형낙여병독진화과정중적각색.방법 이용RT-PCR방법확증5주불동GⅡ.4형낙여병독변이주적의각단백P구서렬,재원핵계통중표체병순화P단백.통과일조HBGAs표형명학적타액양본여P단백결합,진행타액HBGAs결합모식분석.동시,장P단백여인공합성적HBGAs과당진행과당결합분석.결과 타액HBGAs결합모식분석표명,Sakai변이주궤호불결합,기타GⅡ.4변이주적HBGAs결합모식상사,여분비형타액(A、B、AB화O형분비형)결합,여O형비분비형타액불결합.95/96US변이주화2006b변이주결합능력교고,기차시Camberwell변이주,Hunter변이주교약.과당결합분석여타액결합분석결과일치,Sakai변이주불결합,기타독주여균여분비형과당(Ley화H1)결합,여비분비형과당(Lea화Lex)불결합.95/96US변이주화2006b변이주여과당적결합능력교강,기차시Camberwell변이주.결론 절대다수GⅡ.4형낙여병독변이주여HBGAs결합모식상동,단결합능력불동,결합능력강적변이주류행범위교엄.
Objective To investigate the binding profile of the epochal GⅡ.4 norovirus (NoV) variants to the human histo-blood group antigens (HBGAs) and the role of HBGAs in the evolution of the GⅡ.4 NoVs.Methods The sequences of P domain in capsid region of 5 GⅡ.4 NoV variants were amplified by RT-PCR,and P proteins were expressed by protaryotic system and purified.The binding profile of NoV variants to saliva HBGAs was determined by the binding of P protein to a panel of saliva samples which HBGAs phynotypes had been identified previously.The binding profile of oligosaccharide was analyzed by the P protein binding to a panel of synthesized HBGAs oligosaccharide antigens.Results Sakai variant almost lost the binding capacity for saliva HBGAs,and other GⅡ.4 variants had the similar binding profile,which can bind to secretor saliva (A,B,AB and O secretor) and not bind to O non-secretor saliva.95/96US variant and 2006b variant had the highest binding capacities,followed by Camberwell variant and Hunter variant.The oligosaccharide binding profile was consistent with that of saliva HBGAs.Similar to the binding to saliva HBGAs,most variants bound to oligosaccharide secretor (Ley and H1) and did not bind to oligosaccharide secretor (Lea and Lex) except for Sakai variant.95/96US variant and 2006b variant had highest binding capacities,followed by Camberwell variant and Hunter variant,and Sakai variant lost the binding capacity.Conclusions Most GⅡ.4 NoV variants had the similar HBGAs binding profile,but their binding capacities were different,and the variant with high binding capacity caused the epidemic in broader region.
