Table of Contents Author Guidelines Submit a Manuscript
Interdisciplinary Perspectives on Infectious Diseases
Volume 2017, Article ID 4894598, 8 pages
https://doi.org/10.1155/2017/4894598
Review Article

Sulfated Glycans and Related Digestive Enzymes in the Zika Virus Infectivity: Potential Mechanisms of Virus-Host Interaction and Perspectives in Drug Discovery

1Program of Glycobiology, Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, RJ, Brazil
2University Hospital Clementino Fraga Filho, Federal University of Rio de Janeiro, 21941-913 Rio de Janeiro, RJ, Brazil

Correspondence should be addressed to Vitor H. Pomin; rb.jrfu.demqoib@hvnimop

Received 24 October 2016; Accepted 4 January 2017; Published 19 January 2017

Academic Editor: Sandro Cinti

Copyright © 2017 Vitor H. Pomin. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

As broadly reported, there is an ongoing Zika virus (ZIKV) outbreak in countries of Latin America. Recent findings have demonstrated that ZIKV causes severe defects on the neural development in fetuses in utero and newborns. Very little is known about the molecular mechanisms involved in the ZIKV infectivity. Potential therapeutic agents are also under investigation. In this report, the possible mechanisms of action played by glycosaminoglycans (GAGs) displayed at the surface proteoglycans of host cells, and likely in charge of interactions with surface proteins of the ZIKV, are highlighted. As is common for the most viruses, these sulfated glycans serve as receptors for virus attachment onto the host cells and consequential entry during infection. The applications of (1) exogenous sulfated glycans of different origins and chemical structures capable of competing with the virus attachment receptors (supposedly GAGs) and (2) GAG-degrading enzymes able to digest the virus attachment receptors on the cells may be therapeutically beneficial as anti-ZIKV. This communication attempts, therefore, to offer some guidance for the future research programs aimed to unveil the molecular mechanisms underlying the ZIKV infectivity and to develop therapeutics capable of decreasing the devastating consequences caused by ZIKV outbreak in the Americas.