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.

蚊传寨卡病毒（ZIKV）最近在记录有大流行病的南太平洋岛屿和美洲出现。在本研究中，我们调查了结构蛋白C，prM和E在人宿主细胞对ZIKV流行株的容许性中的作用。为此，我们与非洲历史MR766菌株相比，评估了流行菌株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的分子克隆和包含BeH819015结构蛋白区域的MR766的嵌合克隆。我们表明，含有BeH819015结构蛋白的ZIKV在细胞附着中效率低得多，从而导致A549和SH-SY5Y细胞对病毒感染的敏感性降低。