Zika virus is an encapsulated flavivirus that is transmitted by mosquitos. It infects cells by clathrin-mediated endocytosis (CME) and fusion with acidic endosomes . Zika virus requires clathrin-mediated endocytosis and the function of Rab5a . The activation of receptor proteins initiates clathrin-mediated endocytosis. The AP2 linker complex is then recruited to promote clathrin shell assembly and membrane niche formation . As the invagination progresses , dynein (GTPase) oligomerizes around the shoot neck, separating it from the cell surface and generating intracellular vesicles. Vesicles are first transported through the actin's cortex and then along microtubules . The vesicle grows as it goes through the cell. Uncoated vesicles fuse or are transported to early endosomes once the clathrin coating is removed. Vesicle trafficking is regulated by Rab family small membrane GTPases . Confocal microscopy revealed that ZIKV particles were localized in endosomes positive for Rab5 and Rab7. Rab5 and Rab7 silencing prevent ZIKV infection . ZIKV particles are first carried to early Rab5+ endosomes. In contrast, late Rab7+ endosomes may provide a crucial endosomal environment for ZIKV RNA release . All ZIKV strains studied are sensitive to pH values between 6.5 and 6.1 and require endosome acidification to infect . The fusion of the Zika virus occurs in late endosomes and is pH-dependent . NH4Cl, which inhibits endosomal acidification, can prevent Zika virus-containing vesicles from reaching the late stage. Instead, it transports them swiftly to the plasma membrane via a rapid circulation pathway following clathrin-mediated endocytosis . The export of flavivirus particles was discovered to be Lyn-dependent, implying that LC3+ secretory organelles can release vast amounts of virus in a Rab11-dependent way .