Zika virus and neurologic autoimmunity: the putative role of gangliosides

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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.

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Notes from the Field: Evidence of Zika Virus Infection in Brain and Placental Tissues from Two Congenitally Infected Newborns and Two Fetal Losses--Brazil, 2015.

Roosecelis Brasil Martines, Julu Bhatnagar, M Kelly Keating … (2016)

Zika virus is a mosquito-borne flavivirus that is related to dengue virus and transmitted primarily by Aedes aegypti mosquitoes, with humans acting as the principal amplifying host during outbreaks. Zika virus was first reported in Brazil in May 2015 (1). By February 9, 2016, local transmission of infection had been reported in 26 countries or territories in the Americas.* Infection is usually asymptomatic, and, when symptoms are present, typically results in mild and self-limited illness with symptoms including fever, rash, arthralgia, and conjunctivitis. However, a surge in the number of children born with microcephaly was noted in regions of Brazil with a high prevalence of suspected Zika virus disease cases. More than 4,700 suspected cases of microcephaly were reported from mid-2015 through January 2016, although additional investigations might eventually result in a revised lower number (2). In response, the Brazil Ministry of Health established a task force to further investigate possible connections between the virus and brain anomalies in infants (3).

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Peripheral neuropathies and anti-glycolipid antibodies.

Nobuhiro Yuki, H Willison (2002)

This review charts the progress of anti-glycolipid antibodies in neuropathy, from their original discovery 20 years ago in immunoglobulin M paraproteinaemic neuropathy through to current discoveries mapping their relationship to subtypes of Guillain-Barré syndrome. Antibodies to >20 different glycolipids have now been associated with a wide range of clinically identifiable acute and chronic neuropathy syndromes. Particular progress has been achieved in understanding the link between acute motor axonal neuropathy and antibodies to GM1, GD1a, GM1b and GalNAc-GD1a, and between the cranial, bulbar and sensory variants of GBS and antibodies to the disialylated gangliosides GQ1b, GT1a, GD1b and GD3. In addition to clinical and serological studies, the origins and measurement of anti-glycolipid antibodies and their relationships to similar carbohydrate structures on infectious organisms, particularly Campylobacter jejuni, are discussed in the context of a molecular mimicry hypothesis. The structure and nomenclature of relevant glycolipids are outlined, along with information on their localization in nerve, and the influence this has on clinical phenotypes. Major advances have been made in animal modelling of anti-glycolipid antibody-associated diseases, both in vitro and in vivo. This has advanced our understanding of the role of anti-GQ1b antibodies in Miller Fisher syndrome with particular respect to the motor nerve terminal as a potential site of injury, and led to the creation of rabbit models of anti-GD1b and anti-GM1 antibody-mediated sensory and motor neuropathy, respectively. With such information in place, it will now be possible to determine the precise mechanisms by which antibodies injure the different compartments of peripheral nerve and establish how a range of immunomodulating therapies, including current treatments, exert their therapeutic effects. Despite these very significant advances, considerable gaps in our knowledge persist, and it is likely that other pathogenic pathways operate in inflammatory neuropathy that are unrelated to glycolipid antibodies, although these are outside the scope of this review.

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Zika virus infection of the central nervous system of mice.

T Bell, E Field, H Narang (1971)

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Author and article information

Contributors

Juan-Manuel Anaya: anayajm@gmail.com

Carolina Ramirez-Santana: cramirezsantana@gmail.com

Ignacio Salgado-Castaneda: ignaciosalgadoc@hotmail.com

Christopher Chang: chrchang@ucdavis.edu

Aftab Ansari: pathaaa@emory.edu

M. Eric Gershwin: megershwin@ucdavis.edu

Journal

Journal ID (nlm-ta): BMC Med

Journal ID (iso-abbrev): BMC Med

Title: BMC Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1741-7015

Publication date (Electronic): 21 March 2016

Publication date PMC-release: 21 March 2016

Publication date Collection: 2016

Volume: 14

Electronic Location Identifier: 49

Affiliations

[ ]Center for Autoimmune Diseases Research (CREA), Universidad del Rosario, Bogota, Colombia

[ ]Servicio de Neurología, Hospital Central de la Policía, Bogota, Colombia

[ ]Division of Rheumatology, Allergy and Clinical Immunology, University of California Davis, School of Medicine, Davis, CA USA

[ ]Department of Pathology, Emory University School of Medicine, Atlanta, GA USA

Article

Publisher ID: 601

DOI: 10.1186/s12916-016-0601-y

PMC ID: 4802632

PubMed ID: 27001187

SO-VID: 7ee8c40e-e6bc-42f7-a301-8c6b60f63b1c

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Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 12 March 2016

Date accepted : 16 March 2016

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ScienceOpen disciplines: Medicine

Keywords: autoimmunity,gangliosides,guillain-barré syndrome,microcephaly,zika virus

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ScienceOpen disciplines: Medicine

Keywords: autoimmunity, gangliosides, guillain-barré syndrome, microcephaly, zika virus

Zika virus and neurologic autoimmunity: the putative role of gangliosides

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Zika Virus

Most cited references 12

Notes from the Field: Evidence of Zika Virus Infection in Brain and Placental Tissues from Two Congenitally Infected Newborns and Two Fetal Losses--Brazil, 2015.

Peripheral neuropathies and anti-glycolipid antibodies.

Zika virus infection of the central nervous system of mice.

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