Abstract
Zika virus infection is associated with the development of Guillain-Barré syndrome (GBS), a neurological autoimmune disorder caused by immune recognition of gangliosides and other components at nerve membranes. Using a high-throughput ELISA, we have analyzed the anti-glycolipid antibody profile, including gangliosides, of plasma samples from patients with Zika infections associated or not with GBS in Salvador, Brazil. We have observed that Zika patients that develop GBS present higher levels of anti-ganglioside antibodies when compared to Zika patients without GBS. We also observed that a broad repertoire of gangliosides was targeted by both IgM and IgG anti-self antibodies in these patients. Since Zika virus infects neurons, which contain membrane gangliosides, antigen presentation of these infected cells may trigger the observed autoimmune anti-ganglioside antibodies suggesting direct infection-induced autoantibodies as a cause leading to GBS development. Collectively, our results establish a link between anti-ganglioside antibodies and Zika-associated GBS in patients.
Highlights
Zika virus is an arbovirus of the Flaviviridae family, which like dengue viruses and alphavirus chikungunya virus is transmitted by Aedes mosquitoes
Zika virus infection can trigger the development of Guillain Barresyndrome (GBS), a neurological autoimmune disorder mediated by antibodies recognizing gangliosides in nerve membranes
Mechanisms such as molecular mimicry have been identified as a cause for GBS development in certain infections, such as Campylobacter jejuni, but the broad self reactivity observed during GBS suggests a role for alternative mechanisms
Summary
Zika virus is an arbovirus (arthropod-borne) of the Flaviviridae family, which like dengue viruses and alphavirus chikungunya virus is transmitted by Aedes mosquitoes. Discovered in 1947 in Uganda, the first large Zika virus outbreak was reported in Micronesia in 2007 [1] followed by the 2014 French Polynesia outbreak [2] and the massive Latin American outbreak in 2015, which was first reported in Brazil and spread across the Americas [3]. During this outbreak, alarming Zika-associated complications, such as microcephaly and Guillain Barresyndrome (GBS) were reported [4, 5]. Zika virus was added to the list of GBS-associated pathogens due to the high incidence reported during the 2015 Latin America outbreak [8]; Zika virus-associated GBS shows anti-gangliosides antibodies (anti-GA1) that cannot be attributed to molecular mimicry [9], as described for C. jejuni [7], suggesting alternative mechanisms for the generation of autoantibodies as a result of Zika infection
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