Zika Virus (ZIKV)- An Overview


Zika virus (ZIKV) is a member of the flavivirus family, which includes other viruses that cause human diseases such as dengue, yellow fever, and West Nile fever. ZIKV was first isolated from a monkey in Uganda in 1947 and has since been associated with sporadic outbreaks in Africa, Asia, and the Pacific islands. In 2015-2016, ZIKV caused a large epidemic in the Americas, where it was linked to congenital malformations and neurological complications.

ZIKV, like other flaviviruses, has a spherical shape with a diameter of about 50 nm. It consists of four main components: a lipid envelope, an envelope (E) protein, a membrane (M) protein, and a single-stranded positive-sense RNA genome.

The lipid envelope is derived from the host cell membrane and contains embedded E and M proteins. The E protein is the major surface protein that mediates viral attachment, entry, and fusion with host cells. It also elicits neutralizing antibodies and cellular immune responses in the host. The E protein has four domains: a stem transmembrane domain that anchors it to the viral membrane, and three ectodomains (I, II, and III) that form the outer surface of the virus. Domain III is involved in receptor binding, while domains I and II are involved in conformational changes during fusion. The M protein is a smaller protein that lies under the E protein and stabilizes the viral envelope. It is initially synthesized as a precursor protein (prM) that prevents premature fusion of E proteins in the endoplasmic reticulum. The prM protein is cleaved by a host protease during viral maturation in the Golgi apparatus.

The RNA genome of ZIKV is about 10.7 kb long and encodes a single polyprotein that is cleaved by viral and host proteases into three structural proteins (C, prM, and E) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5). The structural proteins form the viral particle, while the non-structural proteins are involved in viral replication, polyprotein processing, and modulation of host immune responses. The RNA genome also has two untranslated regions (UTRs) at the 5` and 3` ends that contain regulatory elements for viral transcription, translation, and replication.

The structure and genome of ZIKV are similar to those of other flaviviruses, but there are also some differences that may affect its pathogenicity and immunogenicity. For instance, ZIKV has unique amino acid substitutions in its E protein that may alter its receptor binding specificity and antigenicity. ZIKV also has a shorter 3` UTR than other flaviviruses that may affect its RNA stability and interaction with host factors. These features may contribute to the unique epidemiology and clinical manifestations of ZIKV infection.