The structural proteins of epidemic and historical strains of Zika virus differ in their ability to initiate viral infection in human host cells
The structural proteins of epidemic and historical strains of Zika virus differ in their ability to initiate viral infection in human host cells
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DOI：
10.1016/j.virol.2017.12.003
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发表时间：
2018-03-01
期刊：
影响因子：
3.7
通讯作者：
Gadea, Gilles
中科院分区：
文献类型：
--
作者：
Bos, Sandra;Viranaicken, Wildriss;Gadea, Gilles
蚊媒寨卡病毒（ZIKV）最近在南太平洋岛屿和美洲出现，并记录了大规模流行病。在本研究中，我们研究了结构蛋白 C、prM 和 E 在人类宿主细胞对 ZIKV 流行株的耐受性中的贡献。为此，我们与非洲历史毒株 MR766 相比，评估了流行毒株 BeH819015 感染上皮 A549 和神经元 SH-SY5Y 细胞的能力。为此，我们生成了 BeH819015 的分子克隆和含有 BeH819015 结构蛋白区域的 MR766 嵌合克隆。我们发现，含有 BeH819015 结构蛋白的 ZIKV 在细胞附着方面的效率要低得多，导致 A549 和 SH-SY5Y 细胞对病毒感染的敏感性降低。我们的数据表明，C、prM 和 E 在 ZIKV 流行株启动人类宿主细胞病毒感染的能力中所起的作用之前被低估了。
Mosquito-borne Zika virus (ZIKV) recently emerged in South Pacific islands and Americas where large epidemics were documented. In the present study, we investigated the contribution of the structural proteins C, prM and E in the permissiveness of human host cells to epidemic strains of ZIKV. To this end, we evaluated the capacity of the epidemic strain BeH819015 to infect epithelial A549 and neuronal SH-SY5Y cells in comparison to the African historical MR766 strain. For that purpose, we generated a molecular clone of BeH819015 and a chimeric clone of MR766 which contains the BeH819015 structural protein region. We showed that ZIKV containing BeH819015 structural proteins was much less efficient in cell-attachment leading to a reduced susceptibility of A549 and SH-SY5Y cells to viral infection. Our data illustrate a previously underrated role for C, prM, and E in ZIKV epidemic strain ability to initiate viral infection in human host cells.