Multiple confounders complicate the calculation of myositis risk with SARS-CoV-2 vaccination

This editorial refers to ‘SARS-CoV-2 vaccination and myositis in Norway and Sweden’, by Rickard Ljung et al., Rheumatology, 2025; https://doi.org/10.1093/rheumatology/keaf609. The global emergency of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic was a landmark event demanding swift adjustment of everyday life, public health and translational research. Vaccine development and deployment became a priority with the recognition that SARS-CoV-2 had high infectivity, that containment measures alone were insufficient, and that there were potentially devastating health and economic impacts from rapid, widespread infection. Technologies using adenovirus vectors (Oxford-AstraZeneca and Janssen) were novel modes of vaccine delivery, while mRNA-based approaches (Pfizer-BioNTech and Moderna) were in use prior to the SARS-CoV-2 pandemic. Widespread SARS-CoV-2 infections and efforts to vaccinate en masse were a unique situation and have generated interest among the public and scientific communities about potential long-term sequelae. Even before the pandemic, controversy existed regarding links between vaccinations and autoimmunity. Theories involving molecular mimicry, bystander activation and adjuvant-induced effects have been proposed but causality has not been demonstrated [1]. Although case reports of autoimmune disease following vaccination exist, epidemiological studies have found only small increases in risk, such as with Guillain-Barré Syndrome following H1N1 influenza vaccination [2]. Overall, the benefits of vaccination have vastly outweighed the small, potential risks of triggering autoimmune diseases.