Palavras-chave
SARS-CoV-2
COVID-19
Autoimunidade
Como Citar
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Resumo
Objetivo: Correlacionar manifestações neurológicas que se enquadrem nos critérios diagnósticos da Síndrome de Guillain-Barré (SGB) após infecção pelo SARS-CoV-2. Revisão bibliográfica: O SARS-CoV-2 pode induzir danos diretos e indiretos em estruturas teciduais, especialmente do Sistema Nervoso Periférico (SNP), ocasionando lesões teciduais, danos neurais, inflamação e até autoimunidade. A extensa liberação de citocinas inflamatórias na infecção causada pelo SARS-CoV-2 pode fazer parte da imunopatologia por trás da ocorrência da SGB pós-Covid-19. O mecanismo de mimetismo molecular viral é descrito como o mais provável na patogênese da SGB a partir da Covid-19. Isso porque os anticorpos produzidos contra glicoproteínas presentes na estrutura do SARS-CoV-2 podem danificar os nervos periféricos do hospedeiro devido à semelhança com as proteínas nativas. Como consequência, há formação de células B e T autorreativas. Sendo assim, os anticorpos formados reagem de maneira cruzada e acabam danificando células do SNP. Considerações finais: A reação inflamatória e a resposta imunológica contra o SARS-CoV-2 podem desencadear síndromes autoimunes como a SGB.
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