Acute‐phase response of human hepatocytes after infection with <i>Chlamydia pneumoniae and</i> cytomegalovirus

Abstract

We conclude that in addition to direct vascular wall infection by C. pneumoniae and CMV, virus-related development of atherosclerosis might also be initiated by chronic liver infection and subsequent production of inflammatory and procoagulant mediators released in the circulation. This may be another pathophysiological link for the observed relation between infections and the development of atherosclerosis.