Influenza A VIRus and Destabilization of Atherosclerotic Carotid Plaques

Atherosclerosis is the main cause of cardiovascular diseases and is characterized by the accumulation of lipids and inflammatory cells such as macrophages and lymphocytes within the vessel wall of large and medium-sized arteries, forming so-called plaques. The underlying molecular mechanisms are not yet clearly understood. In particular, it is not yet clear what factors can cause the "destabilization" of atherosclerotic plaques, thus making them more vulnerable and prone to triggering acute cardiovascular events. Infectious agents have also been implicated in the pathogenesis of atherosclerosis. Some of them would be able to spread from the infected tissue and migrate to endothelial cells, promoting the secretion of inflammatory mediators and the oxidation of low-density lipoproteins (LDL), their accumulation in vascular cells and the formation of foam cells , fundamental mechanisms especially in the formation of vulnerable plaques. Recently, many studies have shown that the influenza virus can also play a role in the destabilization of atherosclerotic plaques. However, the role of influenza A virus (IVA) infection and related vaccination in the destabilization of atherosclerotic plaques is still controversial. Furthermore, the underlying molecular mechanisms are still a matter of investigation. Based on these data, we hypothesized that IV A infection may promote the destabilization of atherosclerotic plaques through a chronic postinfection immune response. This response would lead to systemic and local changes in the expression of pro-atherosclerotic cytokines and chemokines resulting in increased recruitment of monocyte macrophages and upregulation of the expression of scavenger receptors on the surface of macrophages with greater affinity for oxidized LDL (CD36 and Lectins- Like-oxLDL-receptor 1).