Sherman L, Teitz Y
Exp Cell Biol. 1981;49(4):185-94. doi: 10.1159/000163822.
Interferon treatment of Moloney-leukemia-virus-infected cells (3T3/MLV) leads to the formation of virus particles enriched with viral structural glycoproteins, in addition to the inhibition of virus production. A preferential inhibitory effect on incorporation of RNA and proteins rather than glycoproteins was found in the released virus particles from interferon-treated cells. Enrichment in 70,000- and 45,000-dalton glycoprotein (gP-70, gP-45) in these particles was further demonstrated by polyacrylamide analysis of viral proteins pulse-labeled with [3H]-leucine. Viral glycoproteins released as soluble antigens were also determined. A 40% reduction was found in gP-70 and gP-45 released from interferon-treated cells. Radioimmunoprecipitation of pulse-chase-labeled cellular viral proteins showed no effect of interferon on the formation of viral structural 30,000-, 15,000- to 12,000-dalton proteins, and gP-70 and gP-45 from their respective precursors. The uncoordinate effect of interferon inhibition on viral 30,000-dalton protein and gP-70 is discussed.
用干扰素处理莫洛尼白血病病毒感染的细胞(3T3/MLV),除了抑制病毒产生外,还会导致形成富含病毒结构糖蛋白的病毒颗粒。在干扰素处理的细胞释放的病毒颗粒中,发现对RNA和蛋白质而非糖蛋白的掺入有优先抑制作用。通过用[3H]-亮氨酸脉冲标记病毒蛋白的聚丙烯酰胺分析,进一步证明了这些颗粒中70,000道尔顿和45,000道尔顿糖蛋白(gP-70、gP-45)的富集。还测定了作为可溶性抗原释放的病毒糖蛋白。发现从干扰素处理的细胞释放的gP-70和gP-45减少了40%。脉冲追踪标记的细胞病毒蛋白的放射免疫沉淀显示,干扰素对病毒结构30,000道尔顿、15,000至12,000道尔顿蛋白以及gP-70和gP-45从其各自前体的形成没有影响。讨论了干扰素抑制对病毒30,000道尔顿蛋白和gP-70的不协调作用。