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乙型流感病毒对培养的上皮细胞中营养物质转运的影响。

Effect of influenza B virus on nutrient transport in cultured epithelial cells.

作者信息

Gurevitz M, Schulze I T, Swierkosz E M, Arens M Q, Schwarz K B

机构信息

Department of Pediatrics, Cardinal Glennon Children's Hospital, St. Louis, Missouri.

出版信息

Lab Invest. 1987 Dec;57(6):657-64.

PMID:3695411
Abstract

The possibility that influenza virus could induce changes in membrane permeability to nutrients ordinarily concentrated within the cell was examined. Madin-Darby canine kidney cells were infected with egg-grown influenza B virus at 37 degrees C and pH 7.4 (a condition in which influenza virus enters cells by endocytosis). Control cells were mock-infected with allantoic fluid from chick embryos. Transport of phosphate, 2-deoxyglucose, and alpha-aminoisobutyric acid was measured at various intervals, 0 to 10 hours after infection. Uptake of alpha-aminoisobutyric acid and phosphate by infected cells was inhibited at 2 hours as compared with controls, whereas at 6 to 10 hours, the uptake of all nutrients was higher in infected cells. Infected cells preloaded with phosphate or 2-deoxyglucose did not demonstrate increased release of these nutrients. Thus, the virally induced inhibition of uptake early in infection is not a consequence of loss of membrane integrity. Transport studies were also performed in cells with prebound virus exposed to pH 5.0 for 60 seconds at 37 degrees C and then incubated at pH 7.4, at 37 degrees C. Under these conditions, influenza A viruses are known to enter the cell membrane by fusing directly with it and to initiate cell to cell fusion as well. We demonstrated that influenza B virus also caused cell fusion under these conditions. In contradistinction to studies described above at pH 7.4, fused, infected cells demonstrated both marked release and diminished uptake of nutrients as compared with controls. We conclude that influenza B virus does have an effect on host cell membrane permeability; the type of effect seen is markedly influenced by factors known to determine mode of virus entry into the cell.

摘要

研究了流感病毒是否会诱导细胞膜对通常在细胞内浓缩的营养物质的通透性发生变化。将鸡胚培养的乙型流感病毒在37℃和pH 7.4(在这种条件下,流感病毒通过内吞作用进入细胞)下感染Madin-Darby犬肾细胞。对照细胞用来自鸡胚的尿囊液进行模拟感染。在感染后0至10小时的不同时间间隔测量磷酸盐、2-脱氧葡萄糖和α-氨基异丁酸的转运。与对照相比,感染细胞在2小时时对α-氨基异丁酸和磷酸盐的摄取受到抑制,而在6至10小时时,感染细胞对所有营养物质的摄取更高。预先加载磷酸盐或2-脱氧葡萄糖的感染细胞并未表现出这些营养物质释放增加。因此,病毒在感染早期诱导的摄取抑制不是膜完整性丧失的结果。还对预先结合病毒的细胞进行了转运研究,这些细胞在37℃下暴露于pH 5.0 60秒,然后在37℃下于pH 7.4孵育。在这些条件下,已知甲型流感病毒通过直接与细胞膜融合进入细胞膜,并引发细胞间融合。我们证明乙型流感病毒在这些条件下也会引起细胞融合。与上述在pH 7.4条件下的研究不同,融合的感染细胞与对照相比,显示出营养物质的显著释放和摄取减少。我们得出结论,乙型流感病毒确实对宿主细胞膜通透性有影响;所观察到的影响类型明显受已知决定病毒进入细胞方式的因素影响。

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