Laurence L, Roux D, Cailla H, Riviere Y, Marcovistz R, Hovanessian A
Virology. 1985 May;143(1):290-9. doi: 10.1016/0042-6822(85)90116-3.
Intracellular levels of 2',5'-adenyladenosine oligonucleotides were analyzed in different organs of mice during the course of a rabies virus infection. Phosphorylated and nonphosphorylated 2',5'-adenyladenosine oligonucleotides were measured by radioimmunoassay and analyzed further by HPLC. As the infection progressed, concentrations of phosphorylated 2',5'-adenyladenosine oligonucleotides increased strongly, reaching their maxima late in the infection. In contrast, concentrations of the nonphosphorylated 2',5'-adenyladenosine oligonucleotides decreased. A similar phenomenon was observed in spleens analyzed at intervals after treatment of noninfected mice with interferon and poly(I).poly(C) and to a lesser extent after treatment of noninfected mice with interferon and poly(I).poly(C) and to a lesser extent after treatment with poly(I).poly(C) alone, but not after treatment with interferon alone. The products which accumulated during virus infection were primarily phosphorylated dimers whereas during combined interferon and poly(I).poly(C) treatment, the entire range of phosphorylated molecules from dimer to pentamer was present. These data show that infection of mice with rabies virus provokes both the induction and the activation of 2-5A synthetase, as does interferon and poly(I).poly(C) treatment. However, our data indicate that the intracellular products are different in the two situations: the species active on the nuclease were only detected in interferon- and poly(I).poly(C)-treated mice. The absence of molecules able to activate the 2-5A-dependent nuclease in virus-infected mice might well be one of the reasons why the interferon system is ineffective in rabies virus infection.
在狂犬病病毒感染过程中，对小鼠不同器官内2',5'-腺苷酸寡核苷酸的细胞内水平进行了分析。通过放射免疫测定法测量磷酸化和非磷酸化的2',5'-腺苷酸寡核苷酸，并通过高效液相色谱法进一步分析。随着感染的进展，磷酸化的2',5'-腺苷酸寡核苷酸浓度大幅增加，在感染后期达到最大值。相比之下，非磷酸化的2',5'-腺苷酸寡核苷酸浓度下降。在用干扰素和聚肌苷酸-聚胞苷酸（poly(I).poly(C)）处理未感染小鼠后，间隔分析脾脏时也观察到了类似现象，单独用聚肌苷酸-聚胞苷酸处理时程度较轻，但单独用干扰素处理后未观察到该现象。病毒感染期间积累的产物主要是磷酸化二聚体，而在干扰素和聚肌苷酸-聚胞苷酸联合处理期间，存在从二聚体到五聚体的整个磷酸化分子范围。这些数据表明，狂犬病病毒感染小鼠会引发2-5A合成酶的诱导和激活，干扰素和聚肌苷酸-聚胞苷酸处理也会如此。然而，我们的数据表明，两种情况下细胞内产物不同：仅在干扰素和聚肌苷酸-聚胞苷酸处理的小鼠中检测到对核酸酶有活性的物种。病毒感染小鼠中缺乏能够激活2-5A依赖性核酸酶的分子很可能是干扰素系统在狂犬病病毒感染中无效的原因之一。
