Origin of the 1918 Spanish influenza virus: A comparative genomic analysis

Origin of the 1918 Spanish influenza virus: A comparative genomic analysis
复制标题

DOI:
10.1016/j.ympev.2008.02.003
复制
发表时间:
2008-06-01
影响因子:
4.1
通讯作者:
Westover, Kristi M.
Westover, Kristi M.
中科院分区:
生物学1区
文献类型:
--
作者:
Vana, Geoff;Westover, Kristi M.

文献摘要

被引文献

相似文献

为了检验1918年西班牙流感病毒的禽类起源假说,我们调查了广泛分类学分布的流感病毒序列,收集了65个全长基因组,这些基因组代表了禽类、人类和“经典”猪H1N1谱系以及许多其他猪(H1 N2、H3 N1和H3 N2)、人(H2 N2、H3 N2和H5 N1)和禽类(H1N1、H4 N6、H5 N1、H6 N1、H6 N6、H6 N8、H7 N3、H8 N4)。H9 N2和H13 N2)亚型。将来自所有八个区段的氨基酸连接、比对并用于系统发育分析。此外,聚合酶复合物(PB 1,PB 2和PA)的基因进行了单独分析,我们所有的结果表明,Brevig-Mission/1918株在一个位置的基础上,其余的分支含有人类H1N1病毒,并符合重配假说的起源1918年病毒。我们的基因组同源性进一步表明了与“经典”猪H1N1谱系的姐妹关系。单个PB 1、PB 2和PA基因重排与这些基因的重配/重组假设一致。这些结果证明了使用全基因组方法来解决禽源性假说和预测新的大流行性流感毒株出现的重要性。(C)2008年爱思唯尔公司All rights reserved.
To test the avian-origin hypothesis of the 1918 Spanish influenza virus we surveyed influenza sequences from a broad taxonomic distribution and collected 65 full-length genomes representing avian, human and "classic" swine H1N1 lineages in addition to numerous other swine (H1N2, H3N1, and H3N2), human (H2N2, H3N2, and H5N1), and avian (H1N1, H4N6, H5N1, H6N1, H6N6, H6N8, H7N3, H8N4. H9N2, and H13N2) subtypes. Amino acids from all eight segments were concatenated, aligned, and used for phylogenetic analyses. In addition, the genes of the polymerase complex (PB1, PB2, and PA) were analyzed individually, All of our results showed the Brevig-Mission/1918 strain in a position basal to the rest of the clade containing human H1N1s and were consistent with a reassortment hypothesis for the origin of the 1918 virus. Our genome phylogeny further indicates a sister relationship with the "classic" swine H1N1 lineage. The individual PB1, PB2, and PA phylogenies were consistent with reassortment/recombination hypotheses for these genes. These results demonstrate the importance of using a complete-genome approach for addressing the avian-origin hypothesis and predicting the emergence of new pandemic influenza strains. (C) 2008 Elsevier Inc. All rights reserved.