Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Molecular Mimicry between SARS-CoV-2 proteins and human self-antigens related with autoimmune central nervous system (CNS) disorders

Elisa Gouvea Gutman
ORCID logo ,
Renan Amphilophio Fernandes
ORCID logo ,
Jéssica Vasques Raposo-Vedovi
,
Andreza Lemos Salvio
,
Larissa Araujo Duarte
,
Caio Faria Tardim
,
Vinicius Gabriel Coutinho Costa
,
Valeria Coelho Santa Rita Pereira
,
Marcos Martins Da Silva
ORCID logo ,
Fabrícia Lima Fontes-Dantas³
* ,
Soniza Vieira Alves-Leon
* ORCID logo
Version 1 : Received: 30 September 2023 / Approved: 2 October 2023 / Online: 2 October 2023 (11:10:40 CEST)

A peer-reviewed article of this Preprint also exists.

Gutman, E.G.; Fernandes, R.A.; Raposo-Vedovi, J.V.; Salvio, A.L.; Duarte, L.A.; Tardim, C.F.; Costa, V.G.C.; Pereira, V.C.S.R.; Bahia, P.R.V.; da Silva, M.M.; Fontes-Dantas, F.L.; Alves-Leon, S.V. Molecular Mimicry between SARS-CoV-2 Proteins and Human Self-Antigens Related with Autoimmune Central Nervous System (CNS) Disorders. Microorganisms 2023, 11, 2902. Gutman, E.G.; Fernandes, R.A.; Raposo-Vedovi, J.V.; Salvio, A.L.; Duarte, L.A.; Tardim, C.F.; Costa, V.G.C.; Pereira, V.C.S.R.; Bahia, P.R.V.; da Silva, M.M.; Fontes-Dantas, F.L.; Alves-Leon, S.V. Molecular Mimicry between SARS-CoV-2 Proteins and Human Self-Antigens Related with Autoimmune Central Nervous System (CNS) Disorders. Microorganisms 2023, 11, 2902.

Abstract

SARS-CoV-2 can trigger autoimmune central nervous system (CNS) diseases in genetically susceptible individuals, a mechanism poorly understood. Molecular mimicry (MM) has been identified in other viral diseases as potential triggers of autoimmune CNS events. This study investigated if MM is the process through which SARS-CoV-2 induce the breakdown of immune tolerance. The frequency of autoimmune CNS disorders was evaluated in a prospective cohort with patients admitted in the COVID-19 Intense Care Unity (ICU) in Rio de Janeiro. Then, an in silico analysis was performed to identify the conserved regions which share high identity between SARS-Cov-2 anti-gens and human proteins. The sequences with significant identity and antigenic properties were then assessed for their binding capacity to HLA subtypes. Of the 112 patients included, 3 were classified as having an autoimmune disorder. A total of eleven combinations had significant linear and three-dimensional overlap. NMDAR1, MOG and MPO were the self-antigens with more significant combinations, followed by GAD65. All sequences presented at least one epitope with strong or intermediate binding capacity to the HLA subtypes selected. This study underscores the possibility that CNS autoimmune attacks observed in COVID-19 patients, including those in our population, could be driven by MM in genetically predisposed individuals.

Keywords

COVID-19; SARS-CoV-2; Molecular mimicry; immune tolerance; autoimmune disorders; central nervous system.

Subject

Medicine and Pharmacology, Neuroscience and Neurology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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