In vitro selective suppression of feline myeloid colony formation is attributable to molecularly cloned strain of feline leukemia virus with unique long terminal repeat
In vitro selective suppression of feline myeloid colony formation is attributable to molecularly cloned strain of feline leukemia virus with unique long terminal repeat
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DOI：
10.1016/j.rvsc.2004.07.003
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发表时间：
2005-04-01
影响因子：
2.4
通讯作者：
Hasegawa, A
中科院分区：
文献类型：
--
作者：
Nagashima, N;Hisasue, M;Hasegawa, A
对来自患有急性髓细胞白血病（AML）的猫的分子克隆猫白血病病毒（FeLV）-克隆33（C-33）进行了检查，以评估其与AML和骨髓增生异常综合征（MDS）发病机制的关系。为了评价FeLV C-33的体外致病性，对感染FeLV C-33或FeLV亚组A毒株（61 E，一种具有最小致病性的分子克隆毒株）的骨髓细胞进行了骨髓集落形成试验。感染FeLV C-33的猫骨髓单核细胞的髓样集落形成活性显著低于感染61 E的细胞。这表明FeLV C-33对猫具有髓系特异性致病性，FeLV C-33感染可用作研究MDS和AML发病机制的实验模型。(C)2004爱思唯尔有限公司保留所有权利。
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. (C) 2004 Elsevier Ltd. All rights reserved.