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Front. Med. | doi: 10.3389/fmed.2018.00025

Prevalence of IgG autoantibodies against GD3 ganglioside in acute Zika virus infection

  • 1Departamento de Microbiologia Geral, Universidade Federal do Rio de Janeiro, Brazil
  • 2Departamento de Imunologia, Universidade Federal do Rio de Janeiro, Brazil
  • 3Department of Microbiology, New York University School of Medicine, United States
  • 4Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil
  • 5Departamento de Genética, Universidade Federal do Rio de Janeiro, Brazil
  • 6Unidade de Pesquisa Clínica, Fundação Oswaldo Cruz (Fiocruz), Brazil
  • 7Fundação Oswaldo Cruz (Fiocruz), Brazil

Zika virus disease has become a global health emergency with devastating effects on public health. Recent evidences implicate the virus as an emergent neuropathological agent promoting serious pathologies of the human nervous system that include destructive and malformation consequences such as development of ocular and fetal brain lesions, microcephaly in neonates and Guillain–Barré syndrome in adults. These neurological disorders of both the CNS and peripheral nervous systems is thought to be associated to the neurotropic properties of the virus that has ability to infect neural stem cells as well as peripheral neurons, a hallmark of its pathogenicity. The presence of autoantibodies against gangliosides plays a pivotal role in the etiogenesis of Guillain-Barre syndrome as well as peripheral neuropathies and variety of diseases of the nervous system. Gangliosides are a class of galactose-containing cerebrosides mainly expressed in nervous system tissues playing a critical role in the physiology of neural cells and neurogenesis. Herein, our findings indicate that patients at acute phase of Zika virus infection without any neurological signs show increased levels of IgG autoantibody against GD3 gangliosides, a class of glycolipid found to be highly expressed in neural stem cell acting in their maintenance of the self-renewal cellular capacity. It is possible that a pathological threshold of these antibodies is only acquired in secondary or subsequent infections. In the light of these evidences, we propose that the target of GD3 by autoimmune responses may possibly has an effect in the neuropathy and neurogenesis disorder seen during Zika virus infection.

Keywords: Zika virus, Gangliosides, Autoimmunity, Autoantibody, infectious diseases

Received: 06 Jun 2017; Accepted: 25 Jan 2018.

Edited by:

Walderez O. Dutra, Universidade Federal de Minas Gerais, Brazil

Reviewed by:

Flore Rozenberg, Université Paris Descartes, France
Theo Araújo-Santos, Federal University of Western Bahia, Brazil
Alexandre M. Vieira Machado, Fiocruz Research Center Renê Rachou, Brazil  

Copyright: © 2018 Nico, Conde, Rivera-Correa, Vasconcelos-dos-Santos, Freire-de-Lima, Arruda, Freire De Lima, Ferreira Júnior, Vasconcelos, Palatnik-de-Sousa, Tanuri, Savino, Todeschini, Rodriguez and Morrot. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Alexandre Morrot, Universidade Federal do Rio de Janeiro, Departamento de Imunologia, Rio de Janeiro, Brazil, morrot@micro.ufrj.br