Publication
Zika virus and neurologic autoimmunity: the putative role of gangliosides.
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- Persistent URL
- Last modified
- 02/20/2025
- Type of Material
- Authors
- Language
- English
- Date
- 2016
- Publisher
- BioMed Central
- Publication Version
- Copyright Statement
- © Anaya et al. 2016. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
- License
- Final Published Version (URL)
- Title of Journal or Parent Work
- ISSN
- 1472-6920
- Volume
- 14
- Start Page
- 49
- End Page
- 49
- Abstract
- An increasing number of severe neurological complications associated with Zika virus (ZIKV), chiefly Guillain-Barré syndrome (GBS) and primary microcephaly, have led the World Health Organization to declare a global health emergency. Molecular mimicry between glycolipids and surface molecules of infectious agents explain most of the cases of GBS preceded by infection, while a direct toxicity of ZIKV on neural cells has been raised as the main mechanism by which ZIKV induces microcephaly. Gangliosides are crucial in brain development, and their expression correlates with neurogenesis, synaptogenesis, synaptic transmission, and cell proliferation. Targeting the autoimmune response to gangliosides may represent an underexploited opportunity to examine the increased incidence of neurological complications related to ZIKV infection.
- Author Notes
- Keywords
- Research Categories
- Health Sciences, Medicine and Surgery
- Health Sciences, Immunology
- Biology, Neuroscience
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