Gottlieb C, Kornfeld S, Schlesinger S
J Virol. 1979 Jan;29(1):344-51. doi: 10.1128/JVI.29.1.344-351.1979.
Two mouse L cell variant lines (CL 3 and CL 6) selected for resistance to the toxic plant lectin ricin were restricted in their ability to replicate the two alphaviruses Sindbis virus and Semliki Forest virus. CL 3 cells have been shown to exhibit increased CMP-sialic acid:glycoprotein sialyltransferase and GM3 synthetase activities, whereas CL 6 cells have been shown to contain decreased UDPgalactose:glycoprotein galactosyltransferase and UDP-N-acetylglucosamine:glycoprotein N-acetylglucosaminyltransferase activities. The adsorption of Sindbis virus to CL 6 cells was considerably reduced, suggesting that the loss or inaccessibility of the receptors for Sindbis virus accounted for a major defect in virus production in these cells. In contrast, CL 3 synthesized Sindbis viral RNA and proteins but were unable to convert the precursor glycoprotein PE2 to the structural protein E2. The cleavage of PE2 to E2 was also blocked in both CL 3 and CL 6 cells infected with Semliki Forest virus.
两种经筛选获得对有毒植物凝集素蓖麻毒素具有抗性的小鼠L细胞变异株系（CL 3和CL 6），在复制两种甲病毒——辛德毕斯病毒和Semliki森林病毒方面能力受限。已证明CL 3细胞表现出CMP-唾液酸：糖蛋白唾液酸转移酶和GM3合成酶活性增加，而CL 6细胞已证明含有UDP-半乳糖：糖蛋白半乳糖基转移酶和UDP-N-乙酰葡糖胺：糖蛋白N-乙酰葡糖胺基转移酶活性降低。辛德毕斯病毒对CL 6细胞的吸附显著减少，这表明辛德毕斯病毒受体的丧失或无法接近是这些细胞中病毒产生的主要缺陷。相比之下，CL 3合成辛德毕斯病毒RNA和蛋白质，但无法将前体糖蛋白PE2转化为结构蛋白E2。在感染Semliki森林病毒的CL 3和CL 6细胞中，PE2向E2的裂解也被阻断。
