EFFECT OF MURINE HOST GENOTYPE ON MCF VIRUS EXPRESSION, LATENCY, AND LEUKEMIA-CELL TYPE OF LEUKEMIAS INDUCED BY FRIEND MURINE LEUKEMIA HELPER VIRUS
EFFECT OF MURINE HOST GENOTYPE ON MCF VIRUS EXPRESSION, LATENCY, AND LEUKEMIA-CELL TYPE OF LEUKEMIAS INDUCED BY FRIEND MURINE LEUKEMIA HELPER VIRUS
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DOI：
10.1016/0042-6822(83)90332-x
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发表时间：
1983-01-01
期刊：
影响因子：
3.7
通讯作者：
NISHIO, J
中科院分区：
文献类型：
--
作者：
CHESEBRO, B;PORTIS, JL;NISHIO, J
用不同的Friend小鼠白血病辅助病毒株（F-MuLV）接种几株小鼠致新生儿白血病，观察其发病时间、白血病器官中主要细胞类型的细胞化学分析，以及用水貂细胞灶或MCF特异性单克隆抗体检测传染性水貂细胞聚焦诱导（MCF）病毒的表达。大多数balb . cndot . b和IRW小鼠出现迅速、严重的贫血和由红细胞组成的肝脾肿大。MCF病毒通常从IRW小鼠肿大的脾脏中分离。C57BL/10小鼠发病率较低，病程较慢。脾肿大、淋巴结病变伴轻度贫血，主要细胞类型为髓细胞（绿白血病）或淋巴细胞。MCF病毒从未从该小鼠株中分离出来。(C57BL / 10同学。IRW)F1小鼠潜伏期为中等，但所有小鼠在8个月时均发病。观察到髓系、淋巴系和一些带有红细胞成分的混合白血病，但我们没有看到IRW和BALB.cntdot.B小鼠典型的严重贫血或纯红细胞受累。无论白血病细胞类型如何，从22%的小鼠中分离出MCF病毒。DBA/2小鼠的疾病模式与C57BL/10相似。IRW)F1小鼠和MCF病毒从6只小鼠中分离出来。用低毒力的F-MuLV B3株接种IRW小鼠产生的疾病潜伏期比F-MuLV 57长，但两种病毒转化的细胞类型相似。从14只小鼠中获得体外细胞系，大多数在体内具有致瘤性。3株细胞系释放传染性MCF病毒，另外3株表达MCF特异性细胞表面抗原，但不释放病毒。8株细胞系不表达MCF感染病毒或病毒抗原。一些细胞系释放感染性的异向性病毒和/或表达被与异向性病毒反应的单克隆抗体识别的异向性MuLV细胞表面抗原。MCF在许多原发性白血病组织以及C57BL/10和（B10）倍的体外源性白血病细胞系中缺乏表达。IRW)F1小鼠提示MCF病毒的产生和表达在某些小鼠品系或某些造血谱系中可能不是白血病发生所必需的。
Leukemias induced by neonatal inoculations of several mouse strains with different strains of Friend murine leukemia helper virus (F-MuLV) were followed for time of disease onset, cytochemical analysis of predominant cell types in leukemic organs and expression of infectious mink cell focus-inducing (MCF) viruses detected by mink cell foci or MCF-specific monoclonal antibodies. Most BALB.cntdot.B and IRW mice had a rapidly appearing, severe anemia and hepatosplenomegaly consisting of erythroid cells. MCF viruses were usually isolated from enlarged spleens of IRW mice. C57BL/10 mice had a lower incidence of disease and much slower course. Splenomegaly and lymphadenopathy with mild anemia were seen, and the predominant cell types were either myeloid (chloroleukemia) or lymphoid. MCF viruses were never isolated from this mouse strain. (C57BL/10 .times. IRW)F1 mice were intermediate in latency, but all mice had disease by 8 mo. Myeloid, lymphoid and some mixed leukemias with an erythroid component were observed, but in no case did we see the severe anemia or pure erythroid involvement typical of IRW and BALB.cntdot.B mice. MCF viruses were isolated from 22% of these mice regardless of leukemia cell type. DBA/2 mice had a disease pattern similar to the (C57BL/10 .times. IRW)F1 mice, and MCF viruses were isolated from 3 of 6 mice tested. Inoculation of IRW mice with the low virulence B3 strain of F-MuLV produced disease with a longer latency than F-MuLV 57, but similar cell types were transformed by both viruses. In vitro cell lines were derived from 14 mice, and most were tumorogenic in vivo. Three lines released infectious MCF virus, and 3 others expressed MCF-specific cell surface antigens but did not release virus. Eight lines expressed no MCF infectious virus or viral antigens. Several lines released infectious xenotropic viruses and/or expressed xenotropic MuLV cell surface antigens recognized by monoclonal antibodies reactive with xenotropic viruses. The lack of MCF expression in many primary leukemic tissues as well as in in vitro derived leukemia cell lines of C57BL/10 and (B10 .times. IRW)F1 mice suggested that MCF virus generation and expression may not be required for leukemogenesis in some mouse strains or in some hemopoietic lineages.