Fig. 4

Potential mechanisms of long COVID. The interplay of multiple neuroimmune and SARS-CoV-2-specific potential mechanisms, including persisting inflammation (A), autoimmunity (B), direct virus-mediated cytotoxicity (C), and the reactivation of other persisting viruses, such as CMV (D), aberrant mitochondrial function (E), endothelial disfunction, and hypercoagulation (F), dysbiosis and changes in microbiome (G) may operate in various combinations following SARS-CoV-2 infection and contribute to long COVID. The inflammation (red dots) seems to be a core component in all these putative mechanisms, inducing disturbed neuroimmune responses and leading to a persistent physiological and neurological alterations, especially but not exclusively in older population

Abbreviations: COVID: coronavirus disease; SARS-CoV-2: severe acute respiratory syndrome coronavirus type 2, CMV: cytomegalovirus.