Shahgasempour S, Woodroffe S B, Sullivan-Tailyour G, Garnett H M
Department of Biological Sciences, University of Wollongong, New South Wales, Australia.
Arch Virol. 1997;142(1):125-38. doi: 10.1007/s007050050063.
Human cytomegalovirus infection of human umbilical vein endothelial cells reduces the ability of these cells to bind to fibronectin, collagen type IV and laminin. This suppression requires active virus, since UV-inactivated virus did not alter the binding ability of these cells to adhere to fibronectin, collagen type IV, and laminin. In an attempt to elucidate the molecular mechanism of this altered interaction, the surface expression of alpha 5 beta 1, alpha 2 beta 1, alpha 3 beta 1, and alpha 6 beta 1 integrins on cytomegalovirus-infected endothelial cells was examined using attachment inhibition assay and flow cytometric analysis. The results presented here show that infection with human cytomegalovirus selectively alters the expression of integrin on human endothelial cells, with the ability to induce downregulation of alpha 5 beta 1 and alpha 2 beta 1 (p = 0.001) and p = 0.03, respectively), while significantly upregulating alpha 6 beta 1 (p = 0.03), and marginally upregulating alpha 3 beta 1 (p = 0.05).
人巨细胞病毒感染人脐静脉内皮细胞会降低这些细胞与纤连蛋白、IV型胶原和层粘连蛋白结合的能力。这种抑制作用需要活性病毒,因为紫外线灭活的病毒不会改变这些细胞与纤连蛋白、IV型胶原和层粘连蛋白的黏附结合能力。为了阐明这种相互作用改变的分子机制,利用黏附抑制试验和流式细胞术分析检测了巨细胞病毒感染的内皮细胞上α5β1、α2β1、α3β1和α6β1整合素的表面表达。此处给出的结果表明,人巨细胞病毒感染会选择性地改变人内皮细胞上整合素的表达,能够分别诱导α5β1和α2β1下调(p = 0.001和p = 0.03),同时显著上调α6β1(p = 0.03),并略微上调α3β1(p = 0.05)。