COVID-19-associated Autoimmune and Inflammatory Diseases: Molecular Mechanisms and the Role of IVIG Therapy

The emergence of SARS-CoV-2 has not only reshaped our understanding of viral pathogenesis but also highlighted its capacity to trigger autoimmune and inflammatory diseases. Accumulating evidence indicates that SARS-CoV-2 infection can lead to a broad spectrum of immune-mediated complications, ranging from well-defined conditions such as Guillain-Barré syndrome, multisystem inflammatory syndrome in children (MIS-C), and systemic lupus erythematosus, to the development of diverse autoantibodies and atypical inflammatory phenotypes. This review synthesizes the current clinical and experimental evidence linking COVID-19 to autoimmune and inflammatory sequelae. We have provided a structured overview on the multifactorial mechanisms underpinning this immune dysregulation, including molecular mimicry, epitope spreading, bystander activation, cytokine storm, host genetic predisposition, and viral genomic variability. Additionally, we discussed the contribution of gut dysbiosis and metabolic reprogramming in shaping aberrant immune responses following infection. Special attention is given to the therapeutic potential of intravenous immunoglobulin (IVIG), which has shown promise in mitigating hyperinflammation and modulating autoimmunity in affected individuals. IVIG can provide therapeutic benefits by diverse mutually nonexclusive mechanisms. By integrating emerging insights across clinical immunology, virology, and host-pathogen interactions, this review aims to advance our understanding of COVID-19-induced immune complications and therapeutic strategies to manage post-COVID autoimmune and inflammatory syndromes.