Host-Virus Interaction of ZIKA Virus in Modulating Disease Pathogenesis

• Type of Material: Article
• Authors: Nanda Kishore Routhu, Emory University; Siddappa Byrareddy, Emory University
• Language: English
• Date: 2017-06-01
• Publisher: SPRINGER
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2017, Springer Science Business Media New York
• Final Published Version (URL): http://dx.doi.org/10.1007/s11481-017-9736-7
• Title of Journal or Parent Work: JOURNAL OF NEUROIMMUNE PHARMACOLOGY
• Volume: 12
• Issue: 2
• Start Page: 219
• End Page: 232
• Keywords: Virus glycosylation; Immunity; RNA-POLYMERASE; COMPLEX-FORMATION; Pharmacology & Pharmacy; WEST-NILE; Neurosciences & Neurology; Host-virus interaction; YELLOW-FEVER; Neurosciences; Zika virus; Life Sciences & Biomedicine; DENGUE VIRUS; CRYSTAL-STRUCTURE; Neuropathogenesis; NONSTRUCTURAL PROTEINS; CEREBRAL ORGANOIDS; NEURAL PROGENITORS; ANTIBODY-DEPENDENT ENHANCEMENT; Science & Technology

Abstract

The Zika virus (ZIKV) is a newly emerging pathogen that has resulted in a worldwide epidemic. It primarily spreads either through infected Aedes aegypti or Aedes albopictus mosquitos leading to severe neurological disorders such as microcephaly and Guillain-Barré syndrome in susceptible individuals. The mode of ZIKV entry into specific cell types such as: epidermal keratinocytes, fibroblasts, immature dendritic cells (iDCs), and stem-cell-derived human neural progenitors has been determined through its major surface envelope glycoprotein. It has been known that oligosaccharides that are covalently linked to viral envelope proteins are crucial in defining host-virus interactions. However, the role of sugars/glycans in exploiting host-immune mechanisms and aiding receptor-mediated virus entry is not well defined. Therefore, this review focuses on host-pathogen interactions to better understand ZIKV pathogenesis.