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首页> 外文期刊>Journal of Virology >Synthesis of type C virus particles from murine-cultured cells induced by iododeoxyuridine. V. Effect of interferon and its interaction with dexamethasone.
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Synthesis of type C virus particles from murine-cultured cells induced by iododeoxyuridine. V. Effect of interferon and its interaction with dexamethasone.

机译：由碘氧基尿苷诱导的小鼠培养细胞的C型病毒颗粒的合成。 V.干扰素的影响及其与地塞米松的相互作用。

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Previous studies have shown that in certain cell systems dexamethasone may enhance the production of type C viruses. Conversely, interferon has been shown to inhibit their production. Both appear to exert their influence late in the viral replication cycle rather than on the synthesis of viral-specific RNA. In this report dexamethasone and interferon have been used to study some aspects of the mechanisms involved in the synthesis of type C viruses in murine K-BALB cells following induction of virus production by iododeoxyuridine. Interferon inhibited production of xenotropic type C virus induced by iododeoxyuridine from K-BALB cells both in the absence and presence of dexamethasone, but it did not affect production of N-tropic type C virus. Exposure of the cells to interferon for longer than 12 h was required for maximum effect. Two types of inhibitory effects were observed: one diminished by dexamethasone when the steroid was added 24 h after interferon removal, and the second resistant to dexamethasone. The concentration of intracellular group-specific antigen was diminshed after interferon and increased after dexamethasone exposure. When induced cells were treated with both interferon and dexamethasone, the intracellular group-specific protein concentration was slightly increased, but virus production was reduced 10-fold compared with induced cells treated with dexamethasone alone. We conclude that interferon and dexamethasone may affect both the synthesis of viral proteins and the assembly or release of virus particles and that dexamethasone can partially nullify the inhibitory activity of interferon. The results also support previous conclusions that the regulatory mechanisms for synthesis of viral proteins and for the release of viral particles may differ and that controls for xenotropic and ecotropic virus formation may not be identical.
机译：以前的研究表明，在某些细胞系统中，地塞米松可以增强C型病毒的产生。相反，干扰素已被证明抑制其生产。两者似乎在病毒复制循环中延迟发挥其影响，而不是在易于病毒特异性RNA的合成中。在该报告中，DexameLasone和干扰素已经用于研究在碘脱氧尿苷的诱导病毒产生后鼠K-BALB细胞合成C型病毒的机制的一些方面。干扰素抑制来自k-BALB细胞的碘氧酰亚氨酰诱导的异脱石型病毒的产生，无论是k-BAlb细胞，都不会影响N-热带C病毒的产生。最大效果需要细胞暴露于干扰素以长于12小时。观察到两种类型的抑制作用：当干扰素去除后24小时加入类固醇时，通过地塞米松减少的抑制作用，以及对地塞米松的第二次抗性。细胞内组特异性抗原的浓度在干扰素后均在干扰素后和在地塞米松暴露后增加。当用干扰素和地塞米松处理诱导细胞时，与单独用地塞米松处理的诱导细胞相比，细胞内基团特异性蛋白质浓度略微增加，但病毒产生降低了10倍。我们得出结论，干扰素和地塞米松可能影响病毒蛋白的合成以及病毒颗粒的组装或释放，并且地塞米松可以部分损失干扰素的抑制活性。结果还支持以前的结论，即合成病毒蛋白的调节机制和病毒颗粒的释放可能不同，并且异常和生态缺乏病毒形成的对照可能不相同。

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