Drebot M A, Lee S H, Rozee K R
J Interferon Res. 1984 Spring;4(2):167-72. doi: 10.1089/jir.1984.4.167.
Previous studies by Maheshwari et al. have indicated that vesicular stomatitis virus (VSV) released from interferon (IFN)-treated mouse L-929 (L) cells was structurally defective. Such virions had significantly smaller amounts of glycoprotein (G) and membrane protein (M). Olden et al. recently reported, however, that they were not able to repeat the findings of Maheshwari et al. We have examined the effect of IFN on VSV released from three different cell lines and observed that treatment of L-cells and secondary mouse embryo (ME) cells with an amount of mouse IFN that reduced infectious virus yield 100-fold, led to the release of VSV with reduced amounts of G and M proteins. However, at concentrations of IFN less than this concentration, this effect was not observed. In contrast, VSV released from human (Hu)IFN-treated primate BSC-1, cells showed no reduction in their G and M protein even at concentrations resulting in 400-fold decreases in infectious virus yield.
马赫什瓦里等人之前的研究表明，从经干扰素（IFN）处理的小鼠L-929（L）细胞释放的水疱性口炎病毒（VSV）在结构上存在缺陷。此类病毒粒子的糖蛋白（G）和膜蛋白（M）含量显著减少。然而，奥尔登等人最近报告称，他们无法重复马赫什瓦里等人的研究结果。我们研究了干扰素对从三种不同细胞系释放的VSV的影响，观察到用一定量的小鼠干扰素处理L细胞和二代小鼠胚胎（ME）细胞，该干扰素可使感染性病毒产量降低100倍，结果导致释放的VSV中G蛋白和M蛋白的含量减少。然而，在低于该浓度的干扰素浓度下，未观察到这种效应。相比之下，从经人（Hu）干扰素处理的灵长类BSC-1细胞释放的VSV，即使在导致感染性病毒产量降低400倍的浓度下，其G蛋白和M蛋白含量也未减少。
