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Zika virus and neurologic autoimmunity: The putative role of gangliosides

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

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Fecha
2016

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BioMed Central Ltd.

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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. © 2016 Anaya et al.
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Ganglioside , Ganglioside gd 1a , Ganglioside gd 1b , Ganglioside gm1 , Ganglioside gt1 , Unclassified drug , Ganglioside , Article , Autoimmunity , Brain development , Flavivirus , Flavivirus infection , Guillain barre syndrome , Human , Immune response , Immunopathogenesis , Microcephaly , Molecular mimicry , Nerve cell , Neurotropism , Zika virus , Autoimmunity , Brain , Guillain barre syndrome , Immunology , Microcephaly , Pathogenicity , Virology , Zika fever , Zika virus , Autoimmunity , Brain , Gangliosides , Guillain-barre syndrome , Humans , Microcephaly , Molecular mimicry , Zika virus , Zika virus infection , Autoimmunity , Gangliosides , Guillain-barré syndrome , Microcephaly , Zika virus
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