期刊
SCIENCE
卷 358, 期 6365, 页码 933-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aam7120
关键词
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资金
- National Natural Science Foundation of China (NSFC) [31770190, 31730108, 31430037, 81661148054, 81661130162]
- National Key Research and Development Project of China [2016YFD0500304]
- National Science and Technology Major Project of China [2017ZX09101005, 2014CB942801, 2017ZX10304402]
- CAS [QYZDJ-SSW-SMC007, GJHZ1827]
- Shanghai Science and Technology Committee [16JC1420500]
- Beijing Brain Project [Z161100002616004]
- Innovative Research Group from NSFC [81522025, 81621005]
- U.K. Academy of Medical Sciences
- Taishan Scholars program of Shandong province [ts201511056]
Zika virus (ZIKV) has evolved into a global health threat because of its unexpected causal link to microcephaly. Phylogenetic analysis reveals that contemporary epidemic strains have accumulated multiple substitutions from their Asian ancestor. Here we show that a single serine-to-asparagine substitution [Ser(139)-> Asn(139) (S139N)] in the viral polyprotein substantially increased ZIKV infectivity in both human and mouse neural progenitor cells (NPCs) and led to more severe microcephaly in the mouse fetus, as well as higher mortality rates in neonatal mice. Evolutionary analysis indicates that the S139N substitution arose before the 2013 outbreak in French Polynesia and has been stably maintained during subsequent spread to the Americas. This functional adaption makes ZIKV more virulent to human NPCs, thus contributing to the increased incidence of microcephaly in recent ZIKV epidemics.
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