發(fā)布時間：2018-03-16 11:52

  本文選題：流感病毒A型　切入點：HN亞型　出處：《中華疾病控制雜志》2016年11期 　論文類型：期刊論文

【摘要】：目的對一株人感染H9N2禽流感病毒進行高通量測序(next-generation sequencing,NGS)分析,探討其在人群流行的可能性。方法應用高通量測序技術(shù)進行全基因組序列測定(whole genome sequencing,WGS)。對8個基因進行相似性檢索,構(gòu)建系統(tǒng)進化樹并分析其關(guān)鍵位點的分子特征。結(jié)果 8個基因與Gen Bank基因庫相似度最高序列的來源不完全一致,系統(tǒng)進化樹顯示HA基因?qū)儆跉W亞系I群,M基因位于G1-like分支,PB2位于G9-like分支,NA位于一獨立分支,PBl,PA,NP,NS均位于SH/F/98-like分支。HA基因裂解位點為PSRSSR/GLF,226位受體結(jié)合位點為L。除M2基因S31N突變之外,NA基因莖63~65位缺失,PA和PB2基因未發(fā)生L336M和Q591R,E627K等可以增強病毒對哺乳動物適應性的突變,但發(fā)現(xiàn)可以增強病毒毒力的突變?nèi)鏜1基因N30D和T215A,PB2基因L89V,NSl基因P42S。除M2基因S31N突變外,NA基因和M2基因的藥物結(jié)合位點未發(fā)生E119G,R152K,H274Y,R292K和L26F,V27A,A30T,G34E等耐藥性突變。HA和NA糖基化位點預測結(jié)果都有8個糖基化位點,其中分別有7個和5個可靠程度較高。結(jié)論該H9N2禽流感病毒的大部分關(guān)鍵性位點較保守,只有少部分位點發(fā)生一定程度進化與變異,在人群引起流行的可能性不大,但需加強分子方面動態(tài)監(jiān)測。
[Abstract]:Objective to analyze a human H9N2 avian influenza virus (H9N2 avian influenza virus) by high-throughput sequencing next-generation sequencing (NGS) and to explore the possibility of its prevalence in human population. Methods High-throughput sequencing technique was used to determine the whole genome sequencing sequence of the whole genome of H9N2 Avian Influenza virus (H9N2) and to search the similarity of eight genes. The phylogenetic tree was constructed and the molecular characteristics of its key loci were analyzed. The results showed that the source of the highest similarity sequence between the eight genes and the Gen Bank gene pool was not identical. Phylogenetic tree showed that HA gene belongs to Eurasian line I group I, M gene is located in G1-like branch PB2, located in G9-like branch na, located in a separate branch of PBlBlPANPNs, located at SH/F/98-like branch. HA gene cleavage site is PSRSSR-GLF226 receptor binding site, except M2 gene S31N process site. No mutations in L336M and Q591RRNE627K genes could enhance the adaptability of the virus to mammals. However, mutants such as M1 gene N30D and T215AfN PB2 gene L89VGN NSl gene P42S were found to enhance virulence of the virus. Except for M2 gene S31N mutation, there were no drug binding sites of NNA gene and M2 gene. There were no drug binding sites such as E119GfN R152KH274YP292K and L26FV27A3A30TG34E mutation. Ha and na glycosylation sites were not found. All of them had eight glycosylation sites. Conclusion most of the key sites of H9N2 avian influenza virus are conservative, and only a few of them have evolved and mutated to a certain extent. But it is necessary to strengthen molecular dynamic monitoring.
【作者單位】： 中山市疾病預防控制中心檢驗科;
【基金】：廣東省中山市科技計劃項目(2015B1129)
【分類號】：R511.7;R440
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本文編號：1619795