Flanagan J F
J Bacteriol. 1966 Feb;91(2):789-97. doi: 10.1128/jb.91.2.789-797.1966.
Flanagan, John F. (Duke University School of Medicine, Durham. N.C.). Hydrolytic enzymes in KB cells infected with poliovirus and herpes simplex virus. J. Bacteriol. 91:789-797. 1966.-The effect of poliovirus and herpes simplex virus infection on the activity of five hydrolytic enzymes was studied in tissue culture cells of KB type. During the course of poliovirus infection, the activity of beta-glucuronidase, acid protease, acid ribonuclease, acid deoxyribonuclease, and acid phosphatase in the cytoplasm rose to levels two- to fourfold greater than the activity present in the cytoplasm of uninfected cells. The rise in cytoplasmic activity was accompanied by a concomitant decrease in enzymatic activity bound to cell particles. Shift of enzymatic activity from the particulate to soluble state was first detected at 6 hr after poliovirus infection, coinciding with the appearance of new infectious particles and virus cytopathic effect. No net synthesis of these enzymes after poliovirus infection was found. Hydrocortisone added to the culture medium failed to affect either the titer of virus produced in the cells or the release of hydrolytic enzymes from the particulate state. Herpes simplex infection produced minimal alterations in the state of these enzymes in KB cells. It is hypothesized that the breakdown of lysosomes and release of hydrolytic enzymes accompanying poliovirus infection is produced by alterations in cell membrane permeability during the course of virus replication and by the consequent change in the ionic content of the cell sap.
弗拉纳根,约翰·F.(杜克大学医学院,北卡罗来纳州达勒姆)。脊髓灰质炎病毒和单纯疱疹病毒感染的KB细胞中的水解酶。《细菌学杂志》91:789 - 797。1966年。——在KB型组织培养细胞中研究了脊髓灰质炎病毒和单纯疱疹病毒感染对五种水解酶活性的影响。在脊髓灰质炎病毒感染过程中,细胞质中β - 葡萄糖醛酸酶、酸性蛋白酶、酸性核糖核酸酶、酸性脱氧核糖核酸酶和酸性磷酸酶的活性升至未感染细胞细胞质中活性的二至四倍。细胞质活性的升高伴随着与细胞颗粒结合的酶活性的相应降低。脊髓灰质炎病毒感染后6小时首次检测到酶活性从颗粒状态向可溶状态的转变,这与新感染颗粒的出现和病毒细胞病变效应同时发生。未发现脊髓灰质炎病毒感染后这些酶有净合成。添加到培养基中的氢化可的松既不影响细胞中产生的病毒滴度,也不影响水解酶从颗粒状态的释放。单纯疱疹感染对KB细胞中这些酶的状态产生的改变极小。据推测,脊髓灰质炎病毒感染伴随的溶酶体破裂和水解酶释放是由病毒复制过程中细胞膜通透性的改变以及随之而来的细胞液离子含量变化所导致的。