Peterson A J, Nuss D L
J Virol. 1985 Nov;56(2):620-4. doi: 10.1128/JVI.56.2.620-624.1985.
Inoculation of the leafhopper cell line AC-20 with wound tumor virus resulted in a productive noncytopathic infection with no detectable alteration of cellular protein synthesis. Virus-specific polypeptide synthesis, detectable by 8 h postinoculation, increased in a linear fashion, reaching a peak (approximately 10 to 15% of total protein synthesis) by 48 h postinoculation. The rate of viral protein synthesis continued at this level for several days but declined, relative to cellular protein synthesis, as infected cells were passaged. By passage 10, the synthesis of viral polypeptides was reduced to a level approximately 5% of that observed at 48 h postinoculation. Viral protein synthesis was not stimulated by superinfection. Viral antigens and infectious virus persisted in the majority (greater than 90%) of cells in an infected culture even after more than 100 passages. The synthesis of wound tumor virus polypeptides in infected insect vector cells appears to be regulated in a coordinated and selective manner.
用创伤肿瘤病毒接种叶蝉细胞系AC - 20,导致产生性非细胞病变感染,细胞蛋白质合成未检测到改变。接种后8小时可检测到病毒特异性多肽合成,呈线性增加,接种后48小时达到峰值(约占总蛋白质合成的10%至15%)。病毒蛋白质合成速率在该水平持续数天,但随着感染细胞传代,相对于细胞蛋白质合成而下降。到第10代时,病毒多肽合成降至接种后48小时观察到水平的约5%。重复感染不会刺激病毒蛋白质合成。即使经过100多次传代,病毒抗原和感染性病毒仍存在于感染培养物中的大多数(超过90%)细胞中。感染昆虫载体细胞中创伤肿瘤病毒多肽的合成似乎以协调和选择性的方式受到调节。