Chen Guang-Wu, Gong Yu-Nong, Shih Shin-Ru
Department of Computer Science and Information Engineering, School of Electrical and Computer Engineering, College of Engineering, Chang Gung University, Taoyuan, Taiwan; Research Center for Emerging Viral Infections, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Department of Computer Science and Information Engineering, School of Electrical and Computer Engineering, College of Engineering, Chang Gung University, Taoyuan, Taiwan.
J Formos Med Assoc. 2015 May;114(5):456-63. doi: 10.1016/j.jfma.2015.01.015. Epub 2015 Mar 6.
BACKGROUND/PURPOSE: An influenza A pandemic occurred in 2009-2010. A novel H1N1 virus (hereafter H1N1pdm) was responsible for this outbreak. H1N1pdm viruses have been largely seen in recent human influenza A viruses. This virus was descended from a triple-reassorted swine virus consisting of human, avian, and swine origins. As a result, the previously established species-associated signatures could be in jeopardy.
We analyzed all influenza A sequences in the past 5 years after the inclusion of H1N1pdm into human viruses since 2009, and examined how human signatures may lose their distinctness by mixing with avian residues that H1N1pdm have brought in. In particular, we compared how those signatures were changed/shifted in the past 5 years for human-isolated avian influenza A viruses and discussed their implications.
Only eight out of 47 signatures remained human-like for human influenza A viruses in the past 5 years. They are PB2 271A; PB1 336I; PA 356R and 409N; NP 33I, 305K, and 357K; and NS1 227R. Although most avian-like residues were preserved in human-isolated avian influenza A viruses, a number of them were found to have become or on the verge of becoming human-like, including PB2 627, PA 100, 356, 404, 409, NP 33, 61, 305, 357, M2 20, and NS1 81.
Analyzing how species-associated signatures are becoming human-like in human-isolated avian influenza A viruses helps in assessing their potential to go pandemic as well as providing insights into host adaptation.
背景/目的：2009 - 2010年发生了甲型流感大流行。一种新型H1N1病毒（以下简称H1N1pdm）引发了此次疫情。H1N1pdm病毒在近期的人类甲型流感病毒中较为常见。这种病毒源自一种由人类、禽类和猪源组成的三重重组猪病毒。因此，先前确立的物种相关特征可能受到威胁。
我们分析了自2009年H1N1pdm被纳入人类病毒后过去5年的所有甲型流感序列，研究人类特征如何因与H1N1pdm引入的禽类残基混合而失去其独特性。特别是，我们比较了过去5年中人类分离的甲型禽流感病毒的这些特征是如何变化/转移的，并讨论了其意义。
在过去5年中，47个特征中只有8个在人类甲型流感病毒中仍保持人类样特征。它们是PB2 271A；PB1 336I；PA 356R和409N；NP 33I、305K和357K；以及NS1 227R。虽然大多数禽类样残基在人类分离的甲型禽流感病毒中得以保留，但发现其中一些已变得或即将变得像人类特征，包括PB2 627、PA 100、356、404、409、NP 33、61、305、357、M2 20和NS1 81。
分析人类分离的甲型禽流感病毒中物种相关特征如何变得像人类特征，有助于评估其大流行潜力，并深入了解宿主适应性。
