Salzman N P, Sebring E D
J Virol. 1967 Feb;1(1):16-23. doi: 10.1128/JVI.1.1.16-23.1967.
In vaccinia virus-infected cell cultures, cellular protein synthesis was inhibited 50% at 2 hr postinfection (PI) and 80 to 90% by 4 hr PI. Input virus was responsible for this inhibition. Five early proteins, coded for by the viral genome, could be detected at 2 to 3 hr PI. Normally, their synthesis did not continue beyond 6 hr PI, at which time synthesis of a different set of proteins began. When DNA replication was blocked, synthesis of these early proteins continued until 9 to 12 hr PI. The bulk of the proteins which were incorporated into mature virus were synthesized at 8 hr PI and thereafter. The time of their formation was close to the time at which virus maturation occurred. However, 15% of the protein found in mature virus was synthesized early in the infectious cycle. The quantity of "early viral protein" which was not incorporated into mature virus was almost as large as the quantity of viral protein which did appear in mature virus. The "early" and "late" proteins could be shown to have separate and distinct immunological properties. The role of this large quantity of "early" protein is discussed.
在痘苗病毒感染的细胞培养物中，感染后2小时（PI）细胞蛋白质合成被抑制50%，感染后4小时被抑制80%至90%。这种抑制作用是由输入的病毒引起的。感染后2至3小时可检测到由病毒基因组编码的5种早期蛋白质。正常情况下，它们的合成在感染后6小时后就不再继续，此时开始合成另一组不同的蛋白质。当DNA复制被阻断时，这些早期蛋白质的合成会持续到感染后9至12小时。大部分被整合到成熟病毒中的蛋白质在感染后8小时及之后合成。它们形成的时间与病毒成熟的时间接近。然而，在成熟病毒中发现的15%的蛋白质是在感染周期早期合成的。未被整合到成熟病毒中的“早期病毒蛋白”的量几乎与出现在成熟病毒中的病毒蛋白量一样大。“早期”和“晚期”蛋白质具有各自独特的免疫学特性。文中讨论了这种大量“早期”蛋白质的作用。
