Endoplasmic reticulum: a focal point of Zika virus infection

Mohd Ropidi, Muhammad Izzuddin; Khazali, Ahmad Suhail; Nor Rashid, Nurshamimi; Yusof, Rohana

ZIKV is believed to infect cells through receptormediated endocytosis. These putative receptors include Cluster of Differentiation 209 (CD209), Tyrosine-protein kinase receptor Tyro3, and AXL, where overexpression of these receptors in ZIKV-impervious HEK293T cells rendered the cells susceptible to ZIKV infection [13] . In particular, the role of AXL in ZIKV infection has been extensively investigated due to its crucial role in dengue virus infection [13] . During ZIKV infection, AXL mediates ZIKV entry indirectly whereby the phosphatidylserine extension on ZIKV lipid membrane binds to Growth arrest-specific 6 (Gas6), one of the ligands for AXL that serves as a bridge for ZIKV and AXL interaction, resulting in clathrin-mediated virus internalization [14, 15] . The acidic microenvironment within the endosome promotes fusion between the virus envelope proteins and the endosomal membrane resulting in the release of ZIKV genome into the host cell cytosolic space [15, 16] .