Mackow Erich R, Gorbunova Elena E, Gavrilovskaya Irina N
Department of Molecular Genetics and Microbiology, Stony Brook University , Stony Brook, NY, USA.
Front Microbiol. 2015 Jan 5;5:733. doi: 10.3389/fmicb.2014.00733. eCollection 2014.
The endothelium maintains a vascular barrier by controlling platelet and immune cell interactions, capillary tone and interendothelial cell (EC) adherence. Here we suggest common elements in play during viral infection of the endothelium that alter normal EC functions and contribute to lethal hemorrhagic or edematous diseases. In viral reservoir hosts, infection of capillaries and lymphatic vessels may direct immunotolerance without disease, but in the absence of these cognate interactions they direct the delayed onset of human disease characterized by thrombocytopenia and vascular leakage in a severe endothelial dysfunction syndrome. Here we present insight into EC controls of hemostasis, immune response and capillary permeability that are altered by viral infection of the endothelium.
内皮细胞通过控制血小板与免疫细胞的相互作用、毛细血管张力以及内皮细胞间的黏附来维持血管屏障。在此，我们提出在病毒感染内皮细胞过程中发挥作用的共同因素，这些因素会改变内皮细胞的正常功能，并导致致命的出血性或水肿性疾病。在病毒储存宿主中，毛细血管和淋巴管的感染可能导致免疫耐受而不引发疾病，但在缺乏这些同源相互作用的情况下，它们会导致人类疾病延迟发作，其特征为严重的内皮功能障碍综合征中的血小板减少和血管渗漏。在此，我们深入探讨了因内皮细胞病毒感染而改变的内皮细胞对止血、免疫反应和毛细血管通透性的控制。
