Nagashima N, Hisasue M, Nishigaki K, Miyazawa T, Kano R, Hasegawa A
Department of Pathobiology, Nihon University School of Veterinary Medicine, 1866, Kameino, Fujisawa, Kanagawa 252-8510, Japan.
Res Vet Sci. 2005 Apr;78(2):151-4. doi: 10.1016/j.rvsc.2004.07.003.
Molecularly cloned feline leukemia virus (FeLV)-clone 33 (C-33), derived from a cat with acute myelocytic leukemia (AML), was examined to assess its relation to the pathogenesis of AML and myelodysplastic syndrome (MDS). To evaluate in vitro pathogenicity of FeLV C-33, bone marrow colony-forming assay was performed on marrow cells infected with FeLV C-33 or an FeLV subgroup A strain (61E, a molecularly cloned strain with minimal pathogenicity). The myeloid colony-forming activity of feline bone marrow mononuclear cells infected with FeLV C-33 was significantly lower than that of cells infected with 61E. This suggests that FeLV C-33 has myeloid lineage-specific pathogenicity for cats, and that FeLV C-33 infection is useful as an experimental model for investigating pathogenesis of MDS and AML.
对从一只患有急性髓细胞白血病(AML)的猫身上获得的分子克隆猫白血病病毒(FeLV)-克隆33(C-33)进行了检测,以评估其与AML和骨髓增生异常综合征(MDS)发病机制的关系。为了评估FeLV C-33的体外致病性,对感染了FeLV C-33或FeLV A亚群毒株(61E,一种致病性极低的分子克隆毒株)的骨髓细胞进行了骨髓集落形成试验。感染FeLV C-33的猫骨髓单个核细胞的髓系集落形成活性明显低于感染61E的细胞。这表明FeLV C-33对猫具有髓系谱系特异性致病性,并且FeLV C-33感染可作为研究MDS和AML发病机制的实验模型。