Publication

Zika virus and neurologic autoimmunity: the putative role of gangliosides.

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Last modified
  • 02/20/2025
Type of Material
Authors
    Juan-Manuel Anaya, Universidad del RosarioCarolina Ramirez-Santana, Universidad del RosarioIgnacio Salgado-Castaneda, Hospital Central de la PolicíaChristopher Chang, University of California DavisAftab Ansari, Emory UniversityM. Eric Gershwin, University of California Davis
Language
  • English
Date
  • 2016
Publisher
  • BioMed Central
Publication Version
Copyright Statement
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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