Quackenbush S L, Mullins J I, Hoover E A
Department of Pathology, Colorado State University, Fort Collins 80523.
Blood. 1989 Feb;73(2):509-16.
The identification and molecular cloning of a feline leukemia virus (FeLV) isolate (FeLV-FAIDS) that consistently produces immunodeficiency syndrome has allowed prospective investigation of events that occur in the prodromal phase of disease. Using a T-lymphocyte colony forming assay (T-CFU-Ic) we have demonstrated that a drastic depletion of circulating T-CFU-Ic prefigures the development of clinical immunodeficiency disease in inoculated cats and correlates with the appearance and replication of the FeLV-FAIDS variant genome in serially collected bone marrow samples. During the same presymptomatic time period, no significant alterations in conventional mitogen-induced lymphocyte blastogenic responses or in circulating lymphocyte numbers were evident. Thus T-CFU-Ic assay but not conventional mitogen-driven blastogenesis identified animals destined to develop immunodeficiency syndrome. The correlation among T-CFU-Ic depletion, the replication of the lymphocytopathic FeLV-FAIDS variant genome in hematopoietic and lymphoid tissues, and the onset of clinical disease, infers that ablation of a colony-forming T lymphocyte progenitor subset is important in the early pathogenesis of feline retrovirus-induced immunodeficiency syndrome.
一种始终会引发免疫缺陷综合征的猫白血病病毒（FeLV）分离株（FeLV-FAIDS）的鉴定和分子克隆，使得对疾病前驱期所发生事件进行前瞻性研究成为可能。利用T淋巴细胞集落形成试验（T-CFU-Ic），我们已经证明，循环T-CFU-Ic的急剧减少预示着接种猫临床免疫缺陷疾病的发展，并且与连续采集的骨髓样本中FeLV-FAIDS变异基因组的出现和复制相关。在相同的症状出现前时间段内，传统丝裂原诱导的淋巴细胞增殖反应或循环淋巴细胞数量均无明显变化。因此，T-CFU-Ic试验而非传统的丝裂原驱动的细胞增殖鉴定出了注定会发展为免疫缺陷综合征的动物。T-CFU-Ic减少、致淋巴细胞病变的FeLV-FAIDS变异基因组在造血和淋巴组织中的复制以及临床疾病的发作之间的相关性，推断出集落形成T淋巴细胞祖细胞亚群的缺失在猫逆转录病毒诱导的免疫缺陷综合征的早期发病机制中很重要。
