Scientists from Stanford University found how viruses like influenza and SARS-CoV-2 as well as their associated vaccines may increase the risk of heart attack, stroke, heart inflammation, and other heart complications.
The research is published in Circulation Research and was conducted by Patricia Nguyen et al.
Coronary artery disease is a leading cause of morbidity and mortality worldwide.
Once considered primarily a lipid disorder, studies have found that plaque buildup in the heart arteries is composed of immune cells, as well as lipid.
Although flu has long been linked to heart attack and heart inflammation, the recent COVID-19 pandemic has further highlighted the link between viruses and heart complications.
In the study, the team was initially interested in answering the question of how immune cells in living human coronary plaque may contribute to the development of coronary artery disease.
An important immune cell subset found in plaques is the T cell population, the master regulators of all immune cells.
T cells can recruit additional immune cells to sites of inflammation, possess immune memory, and defend the body against repeat attacks by foreign invaders.
Using innovative technologies that enable the interrogation of plaque cells at a single-cell level, the researchers found that memory T cells make up a large proportion of the cell components of the plaque.
Interestingly, a T cell subset known as memory killer (CD8) T cells appeared as clones, suggesting they may bind to a common antigen.
The pattern of clonal expansion of these memory T cells followed coronary artery disease progression, implicating T cells in disease pathology.
The investigators sought to determine the identity of the ligand, which potentially binds and activates the T cell.
They found that the potential T cell receptor ligands matched to peptides from respiratory viruses, including influenza and SARS-CoV-2. This suggested a potential mechanism by which viruses increase heart attack risk.
These findings suggest that a subset of patients may be vulnerable to auto-immune clotting complications induced by previous viral infections.
The development of diagnostic assays to identify these vulnerable patients is critical so that we may develop appropriate prevention and immune-based treatment strategies for these patients.
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