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.
Highlights
Health authorities are on high alert over the spread of the Zika virus (ZIKV)
* Correspondence: anayajm@gmail.com 1Center for Autoimmune Diseases Research (CREA), Universidad del Rosario, Bogota, Colombia Full list of author information is available at the end of the article (GBS) [3,4,5] that prompted the World Health Organization to declare a “public health emergency of international concern” [3]
That there is a role for infection in the pathogenesis of autoimmunity has been clearly demonstrated [11, 14], but the precise mechanism by which disease develops in some individuals but not in others is still not completely clear
Summary
Health authorities are on high alert over the spread of the Zika virus (ZIKV). Autochthonous cases, defined as cases through local onset of disease rather than being acquired from a different location or country and introduced into the community, have been identified in many countries in the Americas. Background Health authorities are on high alert over the spread of the Zika virus (ZIKV). More than 30 countries/territories in the Americas have reported autochthonous, confirmed ZIKV infection cases [1].
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