Maheshwari R K, Husain M M, Friedman R M
Biochem Biophys Res Commun. 1983 Nov 30;117(1):161-8. doi: 10.1016/0006-291x(83)91555-3.
We have investigated the mechanism for the low infectivity of vesicular stomatitis virus (VSV) released from interferon (IFN) -treated cells. With 10-30 units/ml of IFN there was an approximately 5-30 fold reduction in the production of virus particles, as measured by VSV proteins; however, the infectivity of the VSV released from IFN-treated mouse LB, JLS-V9R, or human GM2504 was drastically reduced (2 to 4 logs). The low infectivity of VSV was directly related to a deficiency in virion glycoprotein (G). IFN treatment did not change the specific infectivity of the VSV particles released by HeLa cells; their G protein was also not reduced. A further effect of IFN to reduce the amount of virion M protein appeared to be secondary and was probably not related to the reduced infectivity of VSV.
我们研究了从经干扰素（IFN）处理的细胞中释放的水疱性口炎病毒（VSV）感染性低的机制。使用10 - 30单位/毫升的IFN时，通过VSV蛋白测量，病毒颗粒的产生减少了约5 - 30倍；然而，从经IFN处理的小鼠LB、JLS - V9R或人GM2504细胞中释放的VSV的感染性大幅降低（2至4个对数）。VSV的低感染性与病毒粒子糖蛋白（G）的缺陷直接相关。IFN处理并未改变HeLa细胞释放的VSV颗粒的比感染性；其G蛋白也未减少。IFN降低病毒粒子M蛋白量的进一步作用似乎是次要的，可能与VSV感染性降低无关。
