Structural insight into the Zika virus capsid encapsulating the viral genome
Dear Editor, In 2015, a Zika virus (ZIKV) outbreak began in South and Central America and in the Caribbean, and has since spread to both North America and Asia.1 It has been revealed that ZIKV is the primary cause of severe neurological pathologies, such as neonatal microcephaly and Guillain-Barr(e) syndrome.2 ZIKV infection can also damage mouse testes, posing a potential threat to the mammalian reproductive system.3 Similar to the dengue virus(DENV) and the West Nile virus (WNV), ZIKV is a mosquito-borne flavivirus containing a single-stranded positive-sense RNA genome, which encodes three structural proteins (C, prM/M, and E) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5).2,4,5 The mature form of the flavivirus C protein is ～12kDa, and it plays a critical role in encapsulation of the RNA genome.2 In addition, the C protein interacts with intracellular lipid droplets for viral particle formation2 and inhibits host RNA silencing to suppress the immune response.6 The multiple functions of the flavivirus C protein in the viral life cycle make it an attractive target for drug development.
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We thank Wen Cui and Hongliang Tian for data collection at beamline BL17U1 and BL18U1 of the Shanghai Synchrotron Radiation Facility;Jun Li for data collection at beamline 104 of DIAMOND Synchrotron Radiation Facility;Xia Chen for technical support;Michael Rossmann,Lei Sun,and Erin Weber for discussion and advice. This work was supported by the National Key Basic Research Program of China973 program,2015CB859800;the National Natural Science Foundation of China81772204 and 31528006;the National Key Research Program of China2016YFD0500300
2018-08-29（万方平台首次上网日期，不代表论文的发表时间）
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497-499
