Richardson M A, Boulton R W, Raghow R S, Dalgarno L
Arch Virol. 1980;63(3-4):263-74. doi: 10.1007/BF01315032.
Polypeptide synthesis was examined in mosquito cells during the establishment of a persistent infection with two alphaviruses, Ross River virus (RRV) and Semliki Forest virus (SFV), and in vertebrate cells cytopathically-infected with the same viruses. In Aedes albopictus cell, RRV reached peak titres at 34--48 hours p.i. At 12 hours 85 per cent of cells assayed as infected by infective centre assay; by 48 hours when persistence was established, virus production was reduced and less than 5 per cent of cells assayed as infected. There was no shut-down of host polypeptide synthesis during infection. Viral polypeptide synthesis was maximal between 10 and 24 hours p.i. The major viral polypeptides labelled were nucleocapsid protein and envelope protein(s). The precursor polypeptide p95 which was prominent in infected BHK cells was not detected in mosquito cells. Similar results were obtained on SFV infection. During the establishment of persistence there was a coordinate decline in the synthesis of RRV polypeptides, reaching undetectable levels by 72 hours p.i. Subculturing persitently-infected cells led to a small increase in viral polypeptide synthesis and virus titre. In contrast, during RRV growth in BHK celos host protein synthesis was severly inhibited and by 9--11 hours p.i. virus-specific polypeptide synthesis represented more than 90 per cent of total protein synthetic activity.
在蚊子细胞建立与两种甲病毒,即罗斯河病毒(RRV)和辛德毕斯病毒(SFV)的持续感染过程中,以及在被相同病毒致细胞病变感染的脊椎动物细胞中,对多肽合成进行了检测。在白纹伊蚊细胞中,RRV在感染后34至48小时达到滴度峰值。在感染后12小时,通过感染中心试验检测,85%的细胞被测定为受感染;到48小时建立持续感染时,病毒产生减少,测定受感染的细胞少于5%。感染期间宿主多肽合成未停止。病毒多肽合成在感染后10至24小时达到最大值。标记的主要病毒多肽是核衣壳蛋白和包膜蛋白。在感染的BHK细胞中突出的前体多肽p95在蚊子细胞中未检测到。对SFV感染获得了类似结果。在持续感染建立过程中,RRV多肽合成呈协同下降,到感染后72小时降至检测不到的水平。对持续感染的细胞进行传代培养导致病毒多肽合成和病毒滴度略有增加。相比之下,在BHK细胞中RRV生长期间,宿主蛋白合成受到严重抑制,到感染后9至11小时,病毒特异性多肽合成占总蛋白合成活性的90%以上。