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印度新德里季节性流感 H1N1pdm09 病毒血凝素基因 HA1 结构域的遗传多样性。

Genetic diversity of HA1 domain of hemagglutinin gene of pandemic influenza H1N1pdm09 viruses in New Delhi, India.

机构信息

Department of Microbiology, All India Institute of Medical Sciences, New Delhi, India.

出版信息

J Med Virol. 2012 Mar;84(3):386-93. doi: 10.1002/jmv.23205.

Abstract

Genetic analysis of pandemic 2009 influenza A (H1N1; H1N1pdm09) virus was undertaken to understand virus evolution during 2009 and 2010 in India. Surveillance of influenza viruses from July 2009 to December 2010 revealed major peaks of circulating H1N1pdm09 viruses in August-September and December-January 2009 and then in August-September 2010. To understand the diversity of the H1N1pdm09 virus, selected specimens (n = 23) from 2009 or 2010 were characterized by nucleotide sequence determination of the HA1 subunit of the HA gene. Phylogenetic analysis revealed that 22 clustered with clade 7 viruses characterized by S203T mutations, whereas one virus from 2010 fell within clade 6. None of the viruses from either 2009 or 2010 formed a monophyletic group, suggesting a continuum of independent introduction of circulating viral strains. Amino acid analysis revealed minor amino acid changes in the antigenic or receptor-binding domains. Importantly, we observed mutations that were also present in 1918 pandemic virus, which includes S183P in 4 and S185T mutation in 3 of 13 viruses analyzed from 2010, while none of the 2009 viruses carried these mutations. Whether antibody-mediated pressure is imposing such changes remains to be determined. Continued genetic surveillance is warranted to monitor pathogenicity as the virus evolves to acquire new features.

摘要

对 2009 年甲型流感(H1N1;H1N1pdm09)病毒进行了遗传分析,以了解 2009 年和 2010 年期间病毒的进化情况。对 2009 年 7 月至 2010 年 12 月期间流感病毒的监测显示,循环 H1N1pdm09 病毒于 2009 年 8 月至 9 月和 12 月至 1 月出现了主要高峰,然后于 2010 年 8 月至 9 月再次出现高峰。为了了解 H1N1pdm09 病毒的多样性,对 2009 年或 2010 年的选定标本(n=23)进行了 HA 基因 HA1 亚单位核苷酸序列测定。系统进化分析显示,22 株与 S203T 突变特征的 7 类病毒聚类,而 2010 年的一株病毒属于 6 类。无论是 2009 年还是 2010 年的病毒均未形成单系群,提示循环病毒株的独立传入呈连续状态。氨基酸分析显示在抗原或受体结合结构域发生了微小的氨基酸变化。重要的是,我们观察到了在 1918 年大流行病毒中也存在的突变,包括 2010 年分析的 13 株病毒中的 4 株具有 S183P,3 株具有 S185T 突变,而 2009 年的病毒均无这些突变。抗体介导的压力是否会导致这种变化仍有待确定。随着病毒获得新的特征而不断进化,需要持续进行遗传监测以监测其致病性。

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