Relationship between membrane integrity and the inhibition of host translation in virus-infected mammalian cells. Comparative studies between encephalomyocarditis virus and poliovirus.
Relationship between membrane integrity and the inhibition of host translation in virus-infected mammalian cells. Comparative studies between encephalomyocarditis virus and poliovirus.
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病毒感染的哺乳动物细胞膜完整性与宿主翻译抑制之间的关系。
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发表时间：
1982
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通讯作者：
Luis Carrasco
中科院分区：
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作者：
J. Lacal;Luis Carrasco
研究了微小核糖核酸病毒感染后宿主蛋白质合成的抑制及其与膜通透性改变的关系。在脑心肌炎病毒感染的L细胞中，细胞蛋白质合成从感染后3h开始减少，此时感染细胞对~(86)Rb+的摄取受到抑制。病毒蛋白质的大部分合成发生在离子浓度发生了深刻改变的细胞中。这与理想的病毒翻译需要比细胞蛋白质合成更高浓度的单价离子的观点是一致的。
对EMC病毒感染和脊髓灰质炎病毒感染的HeLa细胞的(A)蛋白质合成、(B)86Rb+含量、(C)膜电位和(D)对潮霉素B的通透性的改变的平行测定表明，在EMC病毒感染的细胞中，膜的变化与宿主蛋白合成的抑制之间存在相关性。这种相关性在脊髓灰质炎病毒感染的细胞中并不明显，这表明在这个系统中，与单价离子变化不同的其他因素参与了关闭。然而，在这个系统中，当细胞膜被修饰并改变对离子的通透性时，病毒蛋白质的合成也发生了。
对感染EMC病毒或脊髓灰质炎病毒的不同细胞系的蛋白质合成和通透性改变的关闭分析表明，关闭的动力学模式是不同的，取决于所使用的细胞系和每个实验中使用的感染的多样性。
在整个感染过程中检测小核糖核酸病毒感染细胞的ATP含量。感染细胞中这种核苷酸的减少从感染后第三个小时开始明显，这一因素可能有助于抑制感染后期发生的病毒蛋白质合成。另一个可能影响这种抑制作用的因素是氨基酸的运输。例如，在感染EMC病毒的细胞中，甘氨酸的转运从感染开始就减少了，在感染后期也观察到蛋氨酸的泄漏。这些膜通透性的改变可能有助于在感染病毒的细胞中观察到的细胞病变效应的发展。
The inhibition of host protein synthesis after picornavirus infection, and its relationship to the modification of membrane permeability has been studied. In encephalomyocarditis (EMC)-virus-infected L cells, cellular protein synthesis is reduced from the third hour after infection, at which time an inhibition in 86Rb+ uptake by the infected cell was observed. The bulk of viral protein synthesis takes place in a cell in which a profound modification in the ionic concentration has occurred. This is in agreement with the idea that optimal viral translation requires a higher concentration of monovalent ions as compared to cellular protein synthesis.
A parallel measurement of (a) protein synthesis, (b) 86Rb+ content, (c) membrane potential and (d) modification of permeability to hygromycin B in EMC-virus-infected and poliovirus-infected HeLa cells, indicates that in EMC-virus-infected cells a correlation exists between membrane alterations and the inhibition of host protein synthesis. This correlation was not apparent in poliovirus-infected cells, suggesting that in this system other factors, different from monovalent ion alterations, are involved in the shut-off. However, in this system, the synthesis of viral proteins also takes place when the cell membrane has been modified and permeability to ions is altered.
The analysis of the shut-off of protein synthesis and permeability modification in different cell lines infected with EMC virus or poliovirus indicates that the kinetic pattern of the shut-off is variable and depends on the cell line used and the multiplicity of infection used in each experiment.
The ATP content of picornavirus-infected cells was examined throughout infection. A decrease of this nucleotide in the infected cells was apparent from the third hour post-infection and this factor could perhaps contribute to the inhibition of viral protein synthesis that occurs late in infection. Another factor that could influence this inhibition is the transport of amino acids. For instance, the transport of glycine decreased from the beginning of the infection in EMC-virus-infected cells and a leakage of methionine was also observed late in infection. These modifications in membrane permeability could contribute to the development of the cytopathic effect observed in virus-infected cells.