Polacino P, Kaplan G, Palma E L
Arch Virol. 1985;86(3-4):291-301. doi: 10.1007/BF01309833.
An attenuated strain of foot-and-mouth disease virus (FMDV) of the A24 Cruzeiro subtype grew less well than wild-type virus in primary bovine fetal kidney (PBK) cells resulting in a 4-log lowered efficiency of plaque formation. Both wild-type and attenuated virus grew equally well in baby hamster kidney (BHK) cells and in suckling mice. Using PBK cells, virus-specific RNA of the wild-type accumulated up to 6 hours after infection. In contrast, PBK cells infected with the attenuated strain made less than 20 per cent of the RNA synthesized by wild-type virus. Infection of the cell with wild-type virus followed by superinfection with attenuated virus led to almost complete inhibition of viral RNA synthesis, an effect which is dependent on the concentration of input attenuated virus. Three subsequent undiluted successive passages of the attenuated virus resulted in a preparation which no longer interfered with wild-type RNA synthesis and which induced more of its own viral RNA synthesis in PBK cells. The basis of this interference was considered. Interference occurred intracellularly and was directed only against viruses within the genus FMDV. A role for interferon was ruled out. Attempts to demonstrate the physical presence of defective interfering (DI) particles of FMDV in the attenuated strain failed; but, cyclic patterns of infectivity were produced during successive undiluted passages.
口蹄疫病毒(FMDV)A24 克鲁塞罗亚型的减毒株在原代牛胎儿肾(PBK)细胞中的生长情况不如野生型病毒,导致空斑形成效率降低 4 个对数。野生型和减毒病毒在幼仓鼠肾(BHK)细胞和乳鼠中生长情况相同。使用 PBK 细胞时,野生型病毒特异性 RNA 在感染后 6 小时内积累。相比之下,感染减毒株的 PBK 细胞合成的 RNA 不到野生型病毒合成量的 20%。先用野生型病毒感染细胞,再用减毒病毒超感染,几乎完全抑制了病毒 RNA 的合成,这种效应取决于输入减毒病毒的浓度。减毒病毒连续三次未稀释传代后,得到的制剂不再干扰野生型 RNA 的合成,并且在 PBK 细胞中诱导产生更多自身的病毒 RNA 合成。对这种干扰的机制进行了探讨。干扰发生在细胞内,且仅针对口蹄疫病毒属内的病毒。排除了干扰素的作用。试图证明减毒株中存在口蹄疫病毒缺陷干扰(DI)颗粒,但未成功;不过,在连续未稀释传代过程中产生了感染性的循环模式。