CAJ | 학술논문

目的探讨2009年广东省新型甲型H1N1流行性感冒(流感)病毒神经氨酸酶(NA)基因的进化及NA基因编码蛋白抗原性、酶活性位点、糖基化位点变异情况.方法从2009年广东省新型甲型H1N1流感患者中分离到病毒毒株共69株,提取病毒总RNA,RT-PCR扩增NA基因,并测序分析;同时从美国国立生物技术信息中心基因库检索获得 52株不同年代、不同地域甲型流感病毒NA基因序列,用MEGA 4.0软件进行基因进化分析和氨基酸序列分析.结果 2009年广东省新型甲型H1N1流感病毒NA基因与禽H5N1流感病毒同源性较高,为87.1%,潜在抗原位点氨基酸分布相同;所有毒株的酶活性中心位点高度保守;具有8个糖基化位点,其中5个位点有不同程度的氨基酸替换,但与2001年禽H5N1毒株的糖基化位点的氨基酸相同.结论 2009年广东省新型甲型H1N1流感病毒NA基因与禽H5N1流感病毒高度同源,与NA抑制剂的特异性结合位点未发生变化.
목적 탐토2009년광동성신형갑형H1N1류행성감모(류감)병독신경안산매(NA)기인적진화급NA기인편마단백항원성、매활성위점、당기화위점변이정황.방법 종2009년광동성신형갑형H1N1류감환자중분리도병독독주공69주,제취병독총RNA,RT-PCR확증NA기인,병측서분석;동시종미국국립생물기술신식중심기인고검색획득 52주불동년대、불동지역갑형류감병독NA기인서렬,용MEGA 4.0연건진행기인진화분석화안기산서렬분석.결과 2009년광동성신형갑형H1N1류감병독NA기인여금H5N1류감병독동원성교고,위87.1%,잠재항원위점안기산분포상동;소유독주적매활성중심위점고도보수;구유8개당기화위점,기중5개위점유불동정도적안기산체환,단여2001년금H5N1독주적당기화위점적안기산상동.결론 2009년광동성신형갑형H1N1류감병독NA기인여금H5N1류감병독고도동원,여NA억제제적특이성결합위점미발생변화.
Objective To analyze the genetic characterization(evolution, antigenicity, enzyme activity sites and glycosylation sites)of the neuraminidase(NA)gene of the novel influenza virus A/H1N1 in 2009 pandemic in Guangdong Province. Methods The viral RNA was extracted from 69 isolates of influenza virus A/H1N1 from patients in 2009 pandemic in Guangdong Province. NA gene fragments were amplified by reverse transcription polymerase chain reaction (RT-PCR) and sequenced. The other 52 NA gene sequences of influenza virus A in different years and different regions were retrieved from GenBank. The analysis of evolution and amino acid sequences were analyzed by MEGA 4.0 software. Results The homology of 2009 novel H1N1 influenza viruses in Guangdong and avian H5N1 influenza virus strains was high(＞85 % ). The amino acid distributions of potential antigenic sites were identical. The enzyme activity sites of NA genes of all virus strains were strictly conserved, which had eight glycosylation sites. But there were amino acid substitutions in 5 glycosylation sites, while it was identical with the 2001 avian H5N1 influenza virus. Conclusion The NA genes of 2009 novel H1N1 influenza viruses in Guangdong are high homologous with avian H5N1 influenza virus and the viral specific binding sites of neuraminidase inhibitor are not changed.