It has been observed during influenza epidemics and in a number of population and clinical trials that this prevalent viral infection was associated with increased death rates from cardiovascular diseases. The clinical and experimental data that may explain accelerated coronary atherosclerosis in influenza infection with implications involving autoimmune mechanisms are analyzed in this article. Both cellular and humoral autoimmune modes could be proposed to participate in the onset or progression of atheromatous lesions due to influenza infection.