GUILLAIN-BARRÉ SYNDROME AFTER VIRAL INFECTION: AN INTEGRATIVE REVIEW OF THE IMMUNOPATHOLOGICAL MECHANISMS INHERENT TO NEUROINFLAMMATORY AUTOIMMUNITY

Abstract

Introduction: Guillain-Barré syndrome (GBS) is an acute immune-mediated peripheral polyneuropathy, often triggered by previous infections. In recent years, emerging viral infections, such as Zika virus and SARS-CoV-2, have been associated with an increased incidence of GBS, reinforcing the role of autoimmune and neuroinflammatory mechanisms in its pathophysiology. Methods: This is an integrative literature review conducted in the National Library of Medicine (PubMed), Medical Literature Analysis and Retrieval System Online (MEDLINE), and ScienceDirect databases. Studies published between 2016 and 2026, in Portuguese or English, that addressed the relationship between viral infections and the immunopathological mechanisms involved in GBS were included. After applying the eligibility criteria, 11 studies comprised the final sample. Results: Observational studies predominated, with a higher frequency of association of GBS with SARS-CoV-2 infection, followed by Zika virus and other flaviviruses. The main mechanisms identified included humoral autoimmune response with production of antiganglioside antibodies, activation of T and B lymphocytes, inflammation mediated by pro-inflammatory cytokines, and, to a lesser extent, direct viral neuroinvasion. Discussion: The findings reinforce molecular mimicry as a central mechanism in viral post-infection GBS, associated with complement activation and axonal or demyelinating injury. Differences in immune profiles appear to influence the clinical variants observed, such as axonal forms and Miller Fisher syndrome. Conclusion: Post-viral infection GBS results from a complex interaction between innate and adaptive immune responses. Understanding these mechanisms is essential for early diagnosis, therapeutic management, and neurological surveillance in the context of emerging viral infections.