VESICULAR STOMATITIS-VIRUS GROWTH IN DROSOPHILA-MELANOGASTER CELLS - G-PROTEIN DEFICIENCY
VESICULAR STOMATITIS-VIRUS GROWTH IN DROSOPHILA-MELANOGASTER CELLS - G-PROTEIN DEFICIENCY
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DOI：
10.1128/jvi.33.1.411-422.1980
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发表时间：
1980-01-01
影响因子：
5.4
通讯作者：
DEZELEE, S
中科院分区：
文献类型：
--
作者：
WYERS, F;RICHARDMOLARD, C;DEZELEE, S
在培养的黑胃d细胞中，水疱性口炎病毒（VSV）建立了一种持续的、非细胞病变的感染。虽然所有细胞最初都被感染，但宿主蛋白合成没有受到抑制。没有检测到有缺陷的干扰粒子，这可以解释载流子态的建立。在果蝇细胞中病毒蛋白合成时间过程的研究中，在感染后1 h内很容易检测到N、NS和M病毒多肽。在病毒周期的任何时候，G蛋白及其前体G1的产量都很低；无论用于感染的VSV毒株或血清型，也无论用作宿主的果蝇细胞系，释放的病毒所含的G总是比鸡胚细胞产生的病毒少4-5倍。感染前加入放线菌素D可使VSV的生长增强8倍。细胞经药物预处理后，G和G1的合成明显高于其他病毒蛋白的合成；然而，释放的病毒表现出与未处理细胞释放的VSV相同的G蛋白缺陷。本文讨论了宿主细胞对G蛋白成熟过程和转录水平合成的控制与G蛋白生物学特性的关系。
In cultured D. melanogaster cells, vesicular stomatitis virus (VSV) established a persistent, noncytopathic infection. No inhibition of host protein synthesis occurred although all cells were initially infected. No defective interfering particles were detected, which would explain the establishment of the carrier state. In studies of the time course of viral protein synthesis in Drosophila cells, N, NS and M viral polypeptides were readily detected within 1 h of infection. The yield of G protein and one of its precursors, G1, was very low at any time of the virus cycle; the released viruses always contained 4-5 times less G than those produced by chicken embryo cells, whatever the VSV strain or serotype used for infection and whatever the Drosophila cell line used as host. Actinomycin D added to the cells before infection enhanced VSV growth up to 8 times. G and G1 synthesis increased much more than that of the other viral proteins when the cells were pretreated with the drug; nevertheless, the released viruses exhibited the same deficiency in G protein as the VSV released from untreated cells. Host cell control on both G-protein maturation process and synthesis at traduction level is discussed in relation to G biological properties.