The researchers studied plaques (cholesterol-containing deposits on blood vessels) and T-cells found in them. They found preliminary evidence that T-cell related autoimmunity contributes to plaques and clotting/thrombotic complications associated with viral infections and vaccines against viruses.
Our finding that plaque T cells display viral specificities is intriguing, especially considering the reports of plaque rupture and myocarditis in healthy individuals receiving the COVID-19 vaccine and in patients infected with influenza and SARS-CoV-2 who may or may not have known cardiovascular comorbidities or even symptoms associated with viral infection.24,29,33 Because these patients are not actively infected based on serological testing (Table S3), they are not producing viral antigens. This raises the question of how T cells specific to virus are activated within the plaque and suggests a potential cross-reactivity of viral epitopes with self-antigens mediating tissue damage, which is otherwise known as molecular mimicry. Although molecular mimicry has been described as a means by which viruses such as influenza or EBV initiate autoimmune diseases,3 its role in atherosclerosis remains unclear.