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Suggested mechanisms for Zika virus causing microcephaly: what do the genomes tell us?

机译:寨卡病毒引起小头畸形的建议机制:基因组告诉我们什么?

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摘要

BackgroundZika virus (ZIKV) is an emerging human pathogen. Since its arrival in the Western hemisphere, from Africa via Asia, it has become a serious threat to pregnant women, causing microcephaly and other neuropathies in developing fetuses. The mechanisms behind these teratogenic effects are unknown, although epidemiological evidence suggests that microcephaly is not associated with the original, African lineage of ZIKV. The sequences of 196 published ZIKV genomes were used to assess whether recently proposed mechanistic explanations for microcephaly are supported by molecular level changes that may have increased its virulence since the virus left Africa. For this we performed phylogenetic, recombination, adaptive evolution and tetramer frequency analyses, and compared protein sequences for the presence of protease cleavage sites, Pfam domains, glycosylation sites, signal peptides, trans-membrane protein domains, and phosphorylation sites.
机译:背景寨卡病毒(ZIKV)是一种新兴的人类病原体。自从非洲经亚洲到达西半球以来,它已成为对孕妇的严重威胁,在发育中的胎儿中引起小头畸形和其他神经病。尽管流行病学证据表明,小头畸形与ZIKV的原始非洲血统无关,但致畸作用背后的机制尚不清楚。使用196种已公布的ZIKV基因组的序列来评估最近提出的针对小头畸形的机制解释是否受到分子水平变化的支持,这种变化可能自病毒离开非洲以来增加了其毒性。为此,我们进行了系统发育,重组,适应性进化和四聚体频率分析,并比较了蛋白质序列中蛋白酶切割位点,Pfam结构域,糖基化位点,信号肽,跨膜蛋白结构域和磷酸化位点的存在。

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