Zika virus and neurologic autoimmunity: The putative role of gangliosides

Juan Manuel Anaya, Carolina Ramirez-Santana, Ignacio Salgado-Castaneda, Christopher Chang, Aftab Ansari, M. Eric Gershwin

Research output: Contribution to journalArticle

39 Scopus citations

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.

Original languageEnglish (US)
Article number49
JournalBMC Medicine
Volume14
Issue number1
DOIs
StatePublished - Mar 21 2016

Keywords

  • Autoimmunity
  • Gangliosides
  • Guillain-Barré syndrome
  • Microcephaly
  • Zika virus

ASJC Scopus subject areas

  • Medicine(all)

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    Anaya, J. M., Ramirez-Santana, C., Salgado-Castaneda, I., Chang, C., Ansari, A., & Gershwin, M. E. (2016). Zika virus and neurologic autoimmunity: The putative role of gangliosides. BMC Medicine, 14(1), [49]. https://doi.org/10.1186/s12916-016-0601-y