Role of ATP in influenza virus budding
Role of ATP in influenza virus budding
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DOI：
10.1006/viro.2001.1181
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发表时间：
2001-11-25
期刊：
影响因子：
3.7
通讯作者：
Nayak, DP
中科院分区：
文献类型：
--
作者：
Hui, EKW;Nayak, DP
流感病毒从病毒感染细胞的质膜上出芽。虽然出芽是病毒复制的关键步骤，但对出芽过程的要求知之甚少。在这份报告中，我们研究了ATP在流感病毒出芽中的作用，通过用一些代谢抑制剂处理流感病毒感染的Madin-Darby犬肾（MDCK）细胞。当WSN病毒感染的MDCK细胞暴露于抗霉素A，羰基氰间氯苯腙，羰基氰对三氟甲氧基苯腙，或寡霉素短时间（15分钟或1小时）的感染周期后期，病毒出芽率下降。这种抑制作用在去除抑制剂后是可逆的。ATP水解的作用进行了分析，通过处理溶血磷脂酰胆碱（LPC）-透性活过滤器生长的病毒感染的MDCK细胞与非渗透性ATP类似物从基底侧和测定病毒出芽从顶侧。在LPC透化的细胞中，膜不可渗透的ATP类似物如腺苷5 ' -O-（3-硫代三磷酸）或5 ' -腺苷酰亚氨基二磷酸导致病毒出芽减少，其可以通过加入过量的ATP而部分恢复。这些数据表明，ATP水解，而不仅仅是ATP结合是病毒出芽所必需的。然而，离子通道（ATP酶）和蛋白质泛素化，这也需要ATP作为能源的抑制剂，不影响流感病毒的出芽，这表明无论是离子通道或蛋白质泛素化活性参与流感病毒出芽。另一方面，用降低膜粘度的二甲基亚砜（DMSO）处理，降低了病毒萌芽的速率，表明膜粘度和膜流动性的物理状态对病毒萌芽有重要影响。报告中提供的数据表明，流感病毒出芽是一个主动的ATP依赖性过程，并表明ATP耗竭和DMSO处理减少病毒出芽可能部分是由于膜粘度降低。(C)北京：科学出版社.
Influenza viruses bud from the plasma membrane of virus-infected cells. Although budding is a critical step in virus replication, little is known about the requirements of the budding process. In this report, we have investigated the role of ATP in influenza virus budding by treating influenza virus infected Madin-Darby canine kidney (MDCK) cells with a number of metabolic inhibitors. When WSN virus-infected MDCK cells were exposed to antimycin A, carbonyl cyanide m-chlorophenylhydrazone, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone, or oligomycin for a short time (15 min or 1 h) late in the infectious cycle, the rate of virus budding decreased. This inhibitory effect was reversible upon removal of the inhibitors. The role of ATP hydrolysis was analyzed by treating lysophosphatidylcholine (LPC)-permeabilized live filter-grown virus-infected MDCK cells with nonpermeable ATP analogues from the basal side and assaying virus budding from the apical side. In LPC-permeabilized cells, membrane-impermeable ATP analogues such as adenosine 5 ' -O-(3-thiotriphosphate) or 5 ' -adenylylimidodiphosphate caused reduction of virus budding which could be partially restored by adding excess ATP. These data demonstrated that ATP hydrolysis and not just ATP binding was required for virus budding. However, inhibitors of ion channel (ATPases) and protein ubiquitinylation, which also required the ATP as energy source, did not affect influenza virus budding, suggesting that neither ion channel nor protein ubiquitinylation activity was involved in influenza virus budding. On the other hand, treatment with dimethyl sulfoxide (DMSO), which decreases membrane viscosity, reduced the rate of virus budding, demonstrating that the physical state of membrane viscosity and membrane fluidity had an important effect on virus budding. Data presented in the report indicate that influenza virus budding is an active ATP-dependent process and suggest that reduced virus budding by ATP depletion and DMSO treatment may be partly due to decreased membrane viscosity. (C) 2001 Academic Press.