Zens W, Degen H J, Barnekow A, Gelderblom H, Jungwirth C
Institut für Virologie und Immunbiologie, Universität Würzburg, Federal Republic of Germany.
Virology. 1989 Aug;171(2):535-42. doi: 10.1016/0042-6822(89)90623-5.
De novo infection of Rous sarcoma virus (RSV) strains of receptor subgroups A, B, C, and D is inhibited by low doses of chick interferon. Adsorption and penetration into the cell are not marginally impaired by interferon treatment. Since the level of proviral DNA synthesis is strongly reduced in the interferon-treated cell it is concluded that uncoating or reverse transcription of the viral genome is inhibited. This inhibition of proviral DNA synthesis is not caused by an arrest of CEF in the stationary phase. Chronic infection of SR-RSV-A, -B, -C, but not SR-RSV-D is also sensitive to interferon. Chick interferon treatment (50 u/ml) also had no inhibitory effect on the amount of transcripts of the RSV-specific oncogene src or the cellular oncogenes src and myc.
低剂量的鸡干扰素可抑制A、B、C和D受体亚组的劳氏肉瘤病毒（RSV）毒株的新生感染。干扰素处理对病毒吸附和进入细胞的过程并无显著损害。由于在经干扰素处理的细胞中前病毒DNA合成水平大幅降低，因此得出结论，病毒基因组的脱壳或逆转录受到了抑制。前病毒DNA合成的这种抑制并非由静止期鸡胚成纤维细胞（CEF）的停滞所致。SR-RSV-A、-B、-C的慢性感染对干扰素敏感，但SR-RSV-D的慢性感染则不然。鸡干扰素处理（50单位/毫升）对RSV特异性癌基因src或细胞癌基因src和myc的转录本数量也没有抑制作用。
