Brune W, Ménard C, Heesemann J, Koszinowski U H
Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Science. 2001 Jan 12;291(5502):303-5. doi: 10.1126/science.291.5502.303.
Human cytomegalovirus infects vascular tissues and has been associated with atherogenesis and coronary restenosis. Although established laboratory strains of human cytomegalovirus have lost the ability to grow on vascular endothelial cells, laboratory strains of murine cytomegalovirus retain this ability. With the use of a forward-genetic procedure involving random transposon mutagenesis and rapid phenotypic screening, we identified a murine cytomegalovirus gene governing endothelial cell tropism. This gene, M45, shares sequence homology to ribonucleotide reductase genes. Endothelial cells infected with M45-mutant viruses rapidly undergo apoptosis, suggesting that a viral strategy to evade destruction by cellular apoptosis is indispensable for viral growth in endothelial cells.
人巨细胞病毒感染血管组织，并与动脉粥样硬化和冠状动脉再狭窄有关。虽然已建立的人巨细胞病毒实验室菌株已丧失在血管内皮细胞上生长的能力，但鼠巨细胞病毒实验室菌株保留了这种能力。通过使用涉及随机转座子诱变和快速表型筛选的正向遗传学方法，我们鉴定出一个控制内皮细胞嗜性的鼠巨细胞病毒基因。这个基因，即M45，与核糖核苷酸还原酶基因具有序列同源性。感染M45突变病毒的内皮细胞迅速发生凋亡，这表明逃避细胞凋亡破坏的病毒策略对于病毒在内皮细胞中的生长是必不可少的。
