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

• Authors: Juan-Manuel Anaya, Universidad del Rosario; Carolina Ramirez-Santana, Universidad del Rosario; Ignacio Salgado-Castaneda, Hospital Central de la Policía; Christopher Chang, University of California Davis; Aftab Ansari, Emory University; M. Eric Gershwin, University of California Davis
• Journal Title: BMC Medical Education
• Volume: Volume 14
• Publisher: BioMed Central | 2016, Pages 49-49
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1186/s12916-016-0601-y
• Subjects: Health Sciences, Immunology; Health Sciences, Medicine and Surgery; Biology, Neuroscience
• Keywords: Autoimmunity; Gangliosides; Guillain-Barré syndrome; Microcephaly; Zika virus; Neurology

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.