Pathophysiology of acute respiratory syndrome coronavirus 2 infection: a systematic literature review to inform EULAR points to consider

Background The SARS-CoV-2 pandemic is a global health problem. Beside the specific pathogenic effect of SARS-CoV-2, incompletely understood deleterious and aberrant host immune responses play critical roles in severe disease. Our objective was to summarise available information on pathophysiology COVID-19. Methods Two reviewers independently identified eligible studies according following PICO framework: P (population): patients with infection; I (intervention): any intervention/no intervention; C (comparator): comparator; O (outcome) clinical or serological outcome including but not limited cell phenotype function serum cytokine concentration. Results Of 55 496 records yielded, 84 articles were for inclusion question-specific research criteria. Proinflammatory expression, interleukin-6 (IL-6), increased, especially COVID-19, although as high other states systemic inflammation. myeloid lymphoid compartments differentially affected by infection depending disease phenotype. Failure maintain interferon (IFN) levels characteristic forms COVID-19 could be related loss-of-function mutations IFN pathway and/or presence anti-IFN antibodies. Antibody response showed variability across individuals spectrum. Multiparametric algorithms variable diagnostic performances predicting survival, hospitalisation, progression severity, mortality. Conclusions affects both humoral cellular immunity severity individual parameters. This systematic literature review informed EULAR ‘points consider’ immunomodulatory therapies.