Santoro M G, Jaffe B M, Garaci E, Esteban M
J Gen Virol. 1982 Dec;63(2):435-40. doi: 10.1099/0022-1317-63-2-435.
Prostaglandins of the A series potently inhibited the production of vaccinia virus in mouse L fibroblasts. With the highest non-toxic dose of PGA1, 4 micrograms/ml, the replication of the virus was inhibited by 95 . 3%. The antiviral activity was dose-dependent and specific for the A series. At the dose used, PGA1 was not toxic to uninfected cells and did not alter cell metabolism as measured by DNA, RNA and protein synthesis. PGA1 did not influence the adsorption of the virus by the host cells and the antiviral activity was not dependent on the presence of PGA1 during the early stages of infection. PGA treatment delayed and partially inhibited virus DNA synthesis and, while it did not produce any change in the pattern of protein synthesis in uninfected cells, it altered both the rate and the pattern of virus protein synthesis. We conclude that PGA1 selectively inhibits one or more steps involved in the replication of vaccinia virus in mouse L fibroblasts.
A 系列前列腺素能有效抑制痘苗病毒在小鼠 L 成纤维细胞中的产生。使用最高无毒剂量的 PGA1(4 微克/毫升)时,病毒复制被抑制了 95.3%。抗病毒活性呈剂量依赖性,且对 A 系列具有特异性。在所使用的剂量下,PGA1 对未感染细胞无毒,并且通过 DNA、RNA 和蛋白质合成测量,不会改变细胞代谢。PGA1 不影响宿主细胞对病毒的吸附,且抗病毒活性不依赖于感染早期阶段 PGA1 的存在。PGA 处理延迟并部分抑制了病毒 DNA 合成,虽然它对未感染细胞的蛋白质合成模式没有产生任何变化,但它改变了病毒蛋白质合成的速率和模式。我们得出结论,PGA1 选择性地抑制了痘苗病毒在小鼠 L 成纤维细胞中复制所涉及的一个或多个步骤。