The nonadaptive nature of the H1N1 2009 Swine Flu pandemic contrasts with the adaptive facilitation of transmission to a new host.
The nonadaptive nature of the H1N1 2009 Swine Flu pandemic contrasts with the adaptive facilitation of transmission to a new host.
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DOI：
10.1186/1471-2148-11-6
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发表时间：
2011-01-06
影响因子：
3.4
通讯作者：
Aris-Brosou S
中科院分区：
文献类型：
--
作者：
Abdussamad J;Aris-Brosou S
在2009年H1N1流感大流行出现之前，最初在猪和人类中传播的病毒发生了多次重新分类事件，但人们对这种新出现的适应性质知之甚少。在这里，我们的分析基于2000年至2010年在北美采集的猪和人类宿主H1N1病毒的1180个完整基因组。我们表明，虽然向人类宿主传播可能需要HA和NA抗原的适应性阶段，但2009年大流行的出现基本上是非适应性的。对NA蛋白的更详细分析表明，2009年的大流行序列具有新的表位和环150中的特定替换，这是与大流行的出现密切相关的非适应性结构变化的原因。由于1918年H1N1大流行病毒中不存在这种替换，我们假设大流行的出现是由于分布在不同区段的地点之间的上位性相互作用。总之，我们的结果与群体动力学模型是一致的，该模型强调了病毒群体中新表位的上位性和非适应性上升，然后当产生的病毒毒力太强时，它们就会消亡。
The emergence of the 2009 H1N1 Influenza pandemic followed a multiple reassortment event from viruses originally circulating in swines and humans, but the adaptive nature of this emergence is poorly understood. Here we base our analysis on 1180 complete genomes of H1N1 viruses sampled in North America between 2000 and 2010 in swine and human hosts. We show that while transmission to a human host might require an adaptive phase in the HA and NA antigens, the emergence of the 2009 pandemic was essentially nonadaptive. A more detailed analysis of the NA protein shows that the 2009 pandemic sequence is characterized by novel epitopes and by a particular substitution in loop 150, which is responsible for a nonadaptive structural change tightly associated with the emergence of the pandemic. Because this substitution was not present in the 1918 H1N1 pandemic virus, we posit that the emergence of pandemics is due to epistatic interactions between sites distributed over different segments. Altogether, our results are consistent with population dynamics models that highlight the epistatic and nonadaptive rise of novel epitopes in viral populations, followed by their demise when the resulting virus is too virulent.
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