Vercellotti G M
Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
Blood Cells. 1990;16(1):209-15; discussion 215-6.
Atherosclerotic lesions have been reported to contain herpes simplex virus (HSV) genomic material. This and other evidence suggests that latent viral infection may be an atherogenic trigger. Moreover, active HSV lesions manifest histologically marked fibrin deposition in microvessels. Our laboratory tested in vitro whether HSV infection would cause human umbilical vein endothelial cells to become procoagulant and attract inflammatory cells. Early infection of human endothelial cells with HSV-1 alters the surface conformation as detected by merocyanine 540 staining. The efficiency of prothrombinase complex assembly increases, resulting in a two- to threefold accelerated rate of thrombin generation on the cell surface of virally infected endothelium. HSV infection of endothelium results in a marked increase in thrombin-induced platelet adhesion with a concomitant decrease in prostacyclin secretion in response to thrombin. Viral infection enhances coagulation by decreasing endothelial thrombomodulin expression and subsequent activation of protein C. Viral infection also induces tissue factor in human endothelial cells within 4 hours of infection. Not only does the endothelial monolayer become procoagulant when infected with HSV, it also becomes a more adherent surface for granulocytes. Resting and stimulated granulocyte adherence is enhanced twofold on virally infected endothelium. Enhanced adhesion is accompanied by excessive granulocyte-mediated lysis of 51Cr-labeled HSV-infected endothelium and endothelial cell detachment from its substrate. Exaggerated endothelial detachment correlated with poor binding of infected endothelial cells to substratum matrix proteins. Resuspended virus-infected cells bound significantly less well to tissue culture containers coated with fibronectin, laminin, and type IV collagen. HSV-infected endothelium alters the anticoagulant properties of the endothelium causing it to become procoagulant.(ABSTRACT TRUNCATED AT 250 WORDS)
据报道，动脉粥样硬化病变中含有单纯疱疹病毒（HSV）基因组物质。这一发现以及其他证据表明，潜伏性病毒感染可能是动脉粥样硬化的触发因素。此外，活跃的HSV病变在组织学上表现为微血管中有明显的纤维蛋白沉积。我们实验室在体外测试了HSV感染是否会导致人脐静脉内皮细胞具有促凝血性并吸引炎症细胞。用HSV-1早期感染人内皮细胞会改变其表面构象，这可通过部花青540染色检测到。凝血酶原酶复合物组装效率提高，导致病毒感染的内皮细胞表面凝血酶生成速率加快两到三倍。HSV感染内皮细胞会导致凝血酶诱导的血小板黏附显著增加，同时凝血酶刺激下的前列环素分泌减少。病毒感染通过降低内皮血栓调节蛋白表达及随后的蛋白C激活来增强凝血。病毒感染还会在感染后4小时内诱导人内皮细胞表达组织因子。当被HSV感染时，内皮单层不仅会变得具有促凝血性，还会成为粒细胞更易黏附的表面。在病毒感染的内皮上，静息和受刺激的粒细胞黏附增强了两倍。增强的黏附伴随着粒细胞介导的对51Cr标记的HSV感染内皮的过度裂解以及内皮细胞从其底物上脱落。内皮细胞过度脱落与感染的内皮细胞与基质蛋白结合不良有关。重悬的病毒感染细胞与涂有纤连蛋白纤连蛋白、层粘连蛋白和IV型胶原的组织培养容器的结合明显较差。HSV感染的内皮改变了内皮的抗凝特性，使其变得具有促凝血性。（摘要截选至250词）
