Vercellotti G M
University of Minnesota Medical School, Minneapolis 55105, USA.
Blood Coagul Fibrinolysis. 1998 Apr;9 Suppl 2:S3-6.
Herpes simplex virus type 1 and cytomegalovirus alter the phenotype of the endothelium in vitro from anticoagulant to procoagulant, thereby promoting the adherence of neutrophils and platelets to the endothelium. Virus infection of the endothelium induces the expression of viral glycoproteins and adhesion molecules, which promote neutrophil and monocyte adhesion. Herpes simplex infection of the endothelium promotes prothrombinase assembly, allowing more efficient thrombin generation. Excess thrombin generation causes translocation of P-selectin. Viral infection also induces the procoagulant molecule, tissue factor, in endothelial cells. These enhanced procoagulant effects are associated with the loss of anticoagulants, including thrombomodulin, prostacyclin and tissue plasminogen activator. These studies support the speculation that virus infection in vivo promotes vascular injury and thrombosis, which may contribute to disease states such as atherosclerosis.
1型单纯疱疹病毒和巨细胞病毒在体外可使内皮细胞的表型从抗凝转变为促凝，从而促进中性粒细胞和血小板与内皮细胞的黏附。内皮细胞的病毒感染会诱导病毒糖蛋白和黏附分子的表达，进而促进中性粒细胞和单核细胞的黏附。内皮细胞的单纯疱疹感染会促进凝血酶原酶组装，使凝血酶生成更高效。过量的凝血酶生成会导致P-选择素移位。病毒感染还会在内皮细胞中诱导促凝分子组织因子。这些增强的促凝作用与抗凝物质的丧失有关，包括血栓调节蛋白、前列环素和组织型纤溶酶原激活剂。这些研究支持了一种推测，即体内病毒感染会促进血管损伤和血栓形成，这可能导致动脉粥样硬化等疾病状态。
