Cytomegalovirus exacerbates atherosclerosis through an autoimmune mechanism

The online, open-access PLoS ONE publishes a new study on the relationship between Cytomegalovirus infection and atherosclerosis, conducted by Prof. Roberto Corrocher and Claudio Lunardi from the University of Verona and by Prof. Antonio Puccetti from the Institute G. Gaslini in Genova, Italy.

The same researchers have already shown that Cytomegalovirus infection can be responsible of the initial vascular lesions typical of the atherosclerotic process. The mechanism involved in the vascular lesion is of autoimmune origin: antibodies directed against particular proteins of the virus are able to bind molecules expressed on the surface of the cells that line the arterial walls (endothelial cells) and to cause their death (apoptosis) through a mechanism called "molecular mimicry."

Using a biocomputational technique, the new study shows that the same anti-Cytomegalovirus antibodies, isolated from patients with coronary artery disease, are able to induce the activation not only of genes involved in apoptosis but also of many other genes that encode for proteins involved in different aspects of the atherosclerotic process (lipid metabolism, inflammation, adhesion molecules, etc.). For the first time, the study shows that one of these proteins is very important because of its ability to activate cells of the innate immune system involved in the initial phases of the disease.

This new study therefore confirms that antibodies directed against Cytomegalovirus-derived proteins purified from patients with coronary artery disease induce endothelial cells damage and support the hypothesis that virus infection plays a crucial role in mediating the atherosclerotic process. Moreover, these findings contribute to the design of novel preventive and therapeutic strategies.

Source: Public Library of Science