Vaquero C, Aujean-Rigaud O, Sanceau J, Falcoff R
Antiviral Res. 1981 Jun;1(2):123-34. doi: 10.1016/0166-3542(81)90038-3.
Infection of mouse L929 cells with Mengo virus resulted in a rapid shut-off of cellular RNA synthesis followed within the first hours post infection by a gradual decrease in host protein synthesis. Pretreatment of the cells with high doses of interferon, blocking viral multiplication, did not affect the virus-induced shut-off of host macromolecular synthesis. In these interferon-treated cells the 2',5'A-activated nuclease may account for the degradation of viral RNA, soon after its replication. However, the inhibition of host protein synthesis could not be explained by this mechanism. Poly(A)-containing RNA, present in interferon-treated and infected cells, amounted to as much as 70% of that present in interferon-treated, noninfected cells. On the other hand, extracted cytoplasmic RNA was efficiently translated in a reticulocyte lysate, showing that extensive mRNA degradation was not involved in the inhibition of host protein synthesis. In the continued presence of interferon, the virus-induced shut-off was found to be transient. Late in infection, RNA synthesis was found to recover, followed by recovery of protein synthesis and survival of the cells.
用门戈病毒感染小鼠L929细胞会导致细胞RNA合成迅速停止，随后在感染后的最初几个小时内宿主蛋白合成逐渐减少。用高剂量干扰素预处理细胞以阻断病毒增殖，并不影响病毒诱导的宿主大分子合成的停止。在这些经干扰素处理的细胞中，2',5'-寡腺苷酸激活的核酸酶可能在病毒RNA复制后不久导致其降解。然而，宿主蛋白合成的抑制不能用这种机制来解释。经干扰素处理并感染的细胞中含多聚腺苷酸的RNA量与经干扰素处理但未感染的细胞中的量一样多，高达70%。另一方面，提取的细胞质RNA在网织红细胞裂解物中能有效翻译，这表明宿主蛋白合成的抑制并不涉及广泛的mRNA降解。在持续存在干扰素的情况下，发现病毒诱导的停止是短暂的。在感染后期，RNA合成恢复，随后蛋白合成恢复，细胞存活。
