Virus infection and cholesterol metabolism in macrophages

Macrophages play a central role in the pathogenesis of atherosclerosis and also are a host for a number of viruses. Cholesterol plays a pivotal role in innate antiviral immune responses. Although impairing innate immune response by increasing cell cholesterol content may be a deliberate strategy used by a pathogen to improve its infectivity, enhancing the risk of atherosclerosis is likely a byproduct. The authors describe in this review various mechanisms enabling viruses to exploit macrophage pathways of cholesterol metabolism, thus diverting cholesterol for a purpose of increasing viral replication and/or for altering innate immune responses. Further elucidation of the mechanisms connecting viral infection and macrophage cholesterol metabolism may be fruitful for developing approaches to treatment of atherosclerosis and viral diseases.