Dietz M, Longley C, Fouchey S P, Hall L, Rich M A, Furmanski P
J Natl Cancer Inst. 1977 Sep;59(3):957-61. doi: 10.1093/jnci/59.3.957.
We characterized several aspects of spontaneous regression of lymphocytic leukemia in mice. The disease, induced by the helper murine leukemia virus (MuLV) component obtained from the regressing Friend virus complex (RFV), was characterized by spleen and lymph node enlargement, thymus involvement, and anemia. Leukemia regression occurred in about 25% of infected mice and resulted in the return of lymphoid organs to near-normal weight and normal histology and the recovery from anemia. A tenfold to 1,000-fold decrease in virus titer was seen in those mice in which leukemia regressed when compared to leukemic animals, although infectious virus was still recoverable from apparently normal spleens. The sera of mice in which leukemia regressed contained potent virus-neutralizing activity that was associated mainly with immunoglobulins. These studies firmly supported the evidence that the regressing phenotype of RFV was due to its helper MuLV component (MuLV-RF).
我们对小鼠淋巴细胞白血病自然消退的几个方面进行了表征。该疾病由从消退型弗氏病毒复合体(RFV)中获得的辅助性鼠白血病病毒(MuLV)成分诱导产生,其特征为脾脏和淋巴结肿大、胸腺受累以及贫血。约25%的感染小鼠出现白血病消退,导致淋巴器官重量恢复至接近正常水平,组织学恢复正常,贫血症状也得以恢复。与白血病动物相比,白血病消退的小鼠病毒滴度下降了10倍至1000倍,尽管从外观正常的脾脏中仍可回收感染性病毒。白血病消退的小鼠血清含有强效的病毒中和活性,主要与免疫球蛋白相关。这些研究有力地支持了以下证据,即RFV的消退表型归因于其辅助性MuLV成分(MuLV-RF)。