Böni J, Böni-Schnetzler M, Frank R M, Franklin R M
Arch Virol. 1986;91(1-2):37-52. doi: 10.1007/BF01316726.
The replication of the avian osteopetrosis virus MAV-2-O was compared in chick embryo fibroblasts from two strains of chicken. These were G-B1 which is relatively resistant to MAV-2-O and CB which is susceptible. The production of MAV-2-O was delayed in G-B1 cells (compared with CB cells). The same result was observed after infection with Rous sarcoma viruses of subgroups B, C, and D. In addition, the transforming viruses induced foci on G-B1 fibroblasts 24 to 48 hours later than on CB fibroblasts. In G-B1 cells there was also a delayed kinetics of intracellular viral RNA production. Integrated and linear unintegrated MAV-2-O DNA species were also present in lower amounts in G-B1 than in CB fibroblasts at 3 days postinfection. In vivo studies confirmed the in vitro situation. There was a marked difference in the amount of virus present in the osteoid bone matrix and the osteocytic lacunae of osteopetrotic bones from susceptible and G-B1 chickens. In contrast to the bone lesions from susceptible animals, budding virus particles were not detectable in lesions from G-B1 chickens. There was no difference in the amount of virus in osteopetrotic and non-osteopetrotic bone of susceptible chickens suggesting that virus replication alone is not sufficient for induction of osteopetrosis and that an additional specific virus-cell interaction is required. The relative resistance of strain G-B1 may therefore, be a consequence of a reduced frequency of this interaction. Its basis may be the lower amount of integrated, as well as unintegrated, viral DNA.
对禽骨质石化病毒MAV-2-O在两种鸡品系的鸡胚成纤维细胞中的复制情况进行了比较。这两种鸡品系分别是对MAV-2-O相对抗性的G-B1和易感的CB。MAV-2-O在G-B1细胞中的产生延迟(与CB细胞相比)。用B、C和D亚组的劳氏肉瘤病毒感染后也观察到了相同的结果。此外,转化病毒在G-B1成纤维细胞上诱导形成病灶的时间比在CB成纤维细胞上晚24至48小时。在G-B1细胞中,细胞内病毒RNA产生的动力学也延迟。感染后3天,整合的和线性未整合的MAV-2-O DNA种类在G-B1中的含量也低于CB成纤维细胞。体内研究证实了体外的情况。在易感鸡和G-B1鸡的骨质石化骨的类骨质骨基质和骨陷窝中存在的病毒量有显著差异。与易感动物的骨病变不同,在G-B1鸡的病变中未检测到出芽的病毒颗粒。易感鸡的骨质石化骨和非骨质石化骨中的病毒量没有差异,这表明仅病毒复制不足以诱导骨质石化,还需要额外的特异性病毒-细胞相互作用。因此,G-B1品系的相对抗性可能是这种相互作用频率降低的结果。其基础可能是整合的以及未整合的病毒DNA含量较低。