前列腺素A抑制水疱性口炎病毒的复制：对病毒糖蛋白的影响。

Prostaglandin A inhibits the replication of vesicular stomatitis virus: effect on virus glycoprotein.

作者信息

Santoro M G, Jaffe B M, Esteban M

出版信息

J Gen Virol. 1983 Dec;64 ( Pt 12):2797-801. doi: 10.1099/0022-1317-64-12-2797.

PMID:6198441

Abstract

Prostaglandins of the A series were found to strongly suppress the replication of vesicular stomatitis virus (VSV) in mouse L fibroblasts. The highest non-toxic dose of PGA1, 4 micrograms/ml, decreased VSV production by 93.6%. At this dose, PGA1 did not alter DNA, RNA or protein synthesis in uninfected L cells for periods up to 24 h, whereas it further suppressed protein synthesis and slightly increased RNA synthesis in VSV-infected cells. The presence of PGA1 during virus adsorption, with no treatment after infection, reduced VSV yields by 63.6%. However, the presence of PGA1 during an early step of VSV replication was not essential for the antiviral action to occur (PGA1 treatment could be started 1 to 2 h post-infection). Apart from a slight overall inhibition of virus protein synthesis, PGA1 strongly suppressed the synthesis of the VSV glycoprotein G; moreover, it produced an alteration in the mobility of this protein in SDS-polyacrylamide gels. We propose that this slight decrease in molecular weight (about 4000) of the G protein in the presence of PGA1 could be due to an alteration in the glycosylation process.

摘要

研究发现，A 系列前列腺素能强烈抑制水泡性口炎病毒（VSV）在小鼠 L 成纤维细胞中的复制。PGA1 的最高无毒剂量为 4 微克/毫升，可使 VSV 产量降低 93.6%。在此剂量下，PGA1 在长达 24 小时的时间内不会改变未感染 L 细胞中的 DNA、RNA 或蛋白质合成，而在 VSV 感染的细胞中，它会进一步抑制蛋白质合成并略微增加 RNA 合成。在病毒吸附期间存在 PGA1，感染后不进行处理，可使 VSV 产量降低 63.6%。然而，在 VSV 复制的早期阶段存在 PGA1 并非抗病毒作用发生的必要条件（PGA1 处理可在感染后 1 至 2 小时开始）。除了对病毒蛋白质合成有轻微的总体抑制作用外，PGA1 还强烈抑制 VSV 糖蛋白 G 的合成；此外，它还使该蛋白在 SDS-聚丙烯酰胺凝胶中的迁移率发生改变。我们认为，在 PGA1 存在的情况下，G 蛋白分子量略有下降（约 4000）可能是由于糖基化过程的改变所致。