Immune activation following cytomegalovirus infection: more important than direct viral effects in cardiovascular disease?
BACKGROUND
Over the last 30 years multiple micro-organisms have been associated with different types of vascular disease, like atherosclerosis, restenosis or transplant arteriosclerosis. Nonetheless, it is still ambiguous which molecular mechanisms are exactly involved in the exacerbating effect of microbes in these disorders.


OBJECTIVE
The present review summarizes sero-epidemiological, in vitro and animal data supporting the role of cytomegalovirus, a member of the herpes virus family, in vascular disease. Additionally, various ways by which the virus can potentially affect the disease will be discussed.


RESULTS
Rodent models as well as in vitro studies suggested that CMV might enhance lesion formation in various ways, like augmentation of the oxLDL uptake, altering monocyte adhesion or increasing the production of pro-inflammatory cytokines. Nevertheless, recent data from our lab and others suggest that alternative mechanisms also may contribute to CMV induced. Inspired by this, we will hypothesise alternative mechanisms by which CMV might affect atherosclerosis.


CONCLUSIONS
Although researchers have tried for many years to unravel the tactics by which micro-organisms, like CMV, aggravate atherosclerosis, so far most suggested mechanisms failed to fully explain both experimental and clinical observations. Therefore, new means to elucidate the observed effects are required.
Stassen
Frank R
FR
Department of Medical Microbiology and Maastricht Infection Center, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 5800, 6202AZ Maastricht, The Netherlands. F.Stassen@medmic.unimaas.nl
Vega-Córdova
Xavier
X
Vliegen
Inge
I
Bruggeman
Cathrien A
CA
D000818:Animals; D050197:Atherosclerosis / Q000276:immunology* / Q000821:virology; D015551:Autoimmunity; D002318:Cardiovascular Diseases / Q000276:immunology* / Q000821:virology*; D003586:Cytomegalovirus Infections / Q000150:complications* / Q000276:immunology*; D006801:Humans; D051193:Toll-Like Receptors / Q000502:physiology
D051193:Toll-Like Receptors