Zika virus (ZIKV) belongs to the family Flaviviridae and genus Flavivirus. It is a singleâstranded positiveâsense ribonucleic acid (RNA) virus, has its origin traced to Zika forest in Uganda. Its infection leads to ZIKV fever, characterized by arthralgia, myalgia, rash, conjunctivitis, and asthenia. Clinical presentation of the infection is nonspecific and may often be confused with symptoms of other flaviviral diseases (dengue, West Nile [WN], and chikungunya). Recently, ZIKV has been associated with congenital malformations and neurological complications such as microcephaly and Guillain–Barre’ syndrome. The viral tropism revealed an infection of the skin fibroblasts, keratinocytes, and immature dendritic cells through enhanced expression of dendritic cellâspecific intracellular adhesion molecule 3âgrabbing nonintegrin or anexelecto (Greekword: 'uncontrolled’) and tyrosine protein kinase receptor 3 systems. Silencing of Tâcell immunoglobulin (Ig) and mucin domain 1 (TIMâ1) and AXL RNAs has shown blockage of viral entry through their antiâTIMâ1 and antiâAXL antibodies, hence serving as a potential target for ZIKV drug development. Biotechnological approaches targeted toward ZIKV vector control include the development of transgenic mosquitoes to disrupt the genome pool of wild strains and use of an endosymbiotic bacterium to prevent replication of arboviruses within its vector. Other approaches include the use of gene drive and exploration of the genetic redundancy to disrupt the receptors used by the virus to gain entry into its host. It is also imperative to explore the modality through which neutralizing antibodies block this viral infection as this may prove as a potential target to arrest the viral life cycle.