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摘要翻译：
2014年初，西非爆发了一种轻微变异的扎伊尔埃博拉亚型，其毒性不如1976年和1994年的菌株。每年的病例数似乎是早期毒株的1000倍，表明传播性大大增强。尽管2014年尖峰糖蛋白突变的比例非常小(~3%)，但死亡率显著降低，而传播似乎大幅增加。生物信息学标度以前在N1(H1N1)和N2(H3N2)流感尖峰糖蛋白突变中显示了类似的毒力和传播的反相关趋势。这些趋势似乎与各种外部因素（移民、纯净水的供应和疫苗接种计划）有关。埃博拉突变反应的分子机制主要涉及其尖峰糖蛋白氨基酸的紊乱粘蛋白样结构域(MLD)的变化。MLD被观察到形成一个低聚两亲楔的尖端，通过氧化机制选择性地撬开细胞-细胞界面。
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英文标题：
《Similarity Is Not Enough: Tipping Points of Ebola Zaire Mortalities》
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作者：
J. C. Phillips
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最新提交年份：
2014
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分类信息：
一级分类：Quantitative Biology 数量生物学
二级分类：Other Quantitative Biology 其他定量生物学
分类描述：Work in quantitative biology that does not fit into the other q-bio classifications
不适合其他q-bio分类的定量生物学工作
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英文摘要：
In early 2014 an outbreak of a slightly mutated Zaire Ebola subtype appeared in West Africa which is less virulent than 1976 and 1994 strains. The numbers of cases per year appear to be ~ 1000 times larger than the earlier strains, suggesting a greatly enhanced transmissibility. Although the fraction of the 2014 spike glycoprotein mutations is very small (~3%), the mortality is significantly reduced, while the transmission appears to have increased strongly. Bioinformatic scaling had previously shown similar inversely correlated trends in virulence and transmission in N1 (H1N1) and N2 (H3N2) influenza spike glycoprotein mutations. These trends appear to be related to various external factors (migration, availability of pure water, and vaccination programs). The molecular mechanisms for Ebola's mutational response involve mainly changes in the disordered mucin-like domain (MLD) of its spike glycoprotein amino acids. The MLD has been observed to form the tip of an oligomeric amphiphilic wedge that selectively pries apart cell-cell interfaces via an oxidative mechanism.
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PDF链接：
https://arxiv.org/pdf/1503.01096
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