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Cited by 292 publications
(133 citation statements)
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References 22 publications
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“…CMV infection causes EC activation with procoagulant effects, increasing the risk of vascular thrombosis (133,(135)(136)(137)(138)(139). In vitro, CMV infection of ECs induces platelet aggregation and adherence and expression of von Willebrand factor (vWF), ICAM1 and VCAM1.…”
Section: Procoagulant Effectsmentioning
confidence: 99%
“…CMV infection causes EC activation with procoagulant effects, increasing the risk of vascular thrombosis (133,(135)(136)(137)(138)(139). In vitro, CMV infection of ECs induces platelet aggregation and adherence and expression of von Willebrand factor (vWF), ICAM1 and VCAM1.…”
Section: Procoagulant Effectsmentioning
confidence: 99%
“…Primary HCMV infection is followed by a life long persistence of the virus in a latent state and reactivation of latent virus is considered to be the major source of virus in immunocompromised individuals (Reeves and Sinclair, this volume). HCMV is linked to the development of arterial restenosis following angioplasty, atherosclerosis, and solid organ TVS (Melnick et al 1983;Speir et al 1994;Melnick et al 1998). HCMV infection nearly doubles the 5-year rate of cardiac graft failure due to accelerated TVS (Grattan et al 1989) and prior to the advent of ganciclovir therapy, doubled the rate of liver graft loss at 3 years (Deotero et al 1998;Rubin 1999).…”
mentioning
confidence: 99%
“…Most of the evidence suggesting an association between infection with the herpes family of viruses (e.g., herpes simplex virus, CMV) and the development of native atherosclerosis or cardiac allograft vasculopathy comes from experimental works (8,15,16,20). Normocholesterolemic chickens with Marek's disease, a disorder caused by an avian herpesvirus infection, developed occlusive atherosclerotic lesions (21).…”
Section: Groupsmentioning
confidence: 99%
“…However, there are data that contradict this hypothesis (11)(12)(13)(14). Whereas many studies have demonstrated possible links between herpesviruses and native atherosclerosis (15)(16)(17)(18), data that demonstrate a relationship between the virus and the development of accelerated graft coronary atherosclerosis are fewer and inconclusive. In this study, we tried to clarify whether HCMV is directly involved in the pathogenesis of accelerated graft coronary atherosclerosis, using the very sensitive techniques of immunohistochemistry (IHC), in situ hybridization (ISH), and polymerase chain reaction in situ (PCR-IS) to locate HCMV antigens or genome in coronary artery segments obtained at necropsies from cardiac allograft recipients.…”
mentioning
confidence: 99%