禽成髓细胞病病毒感染鸡靶组织中原病毒DNA的限制性添加。

M A Baluda, M Shoyab, M Ali, P D Markham, W N Drohan
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引用次数: 2

摘要

原病毒DNA在鸡细胞感染禽流感冠状病毒后一小时内合成,并在短时间内整合到细胞核DNA中。病毒DNA似乎被合成为大约6 X 10(6)道尔顿的双链分子,其中一些被转化为超螺旋环,这可能是整合的必要条件。正常鸡细胞中的内源性v-DNA和白血病鸡成髓细胞中的内源性和amv -DNA都与染色体DNA共价连接。感染后数周,白血病细胞中没有检测到圆形或线状的游离DNA。内源v-DNA由亲本垂直传给子代,在鸡各器官内分布均匀稳定。所有正常细胞的每个单倍体基因组大约有1-2个内源性原病毒拷贝。这种DNA与ravo RNA密切相关。在AMV感染后,靶细胞如白血病髓母细胞、红细胞和肾母细胞似乎获得AMV DNA的完整拷贝。有趣的是,只有这些靶细胞才能在鸡体内和体外转化为肿瘤细胞。除了内源性v-DNA外,靶细胞每个单倍体基因组还获得1-2份AMV特异性DNA。所有现有证据表明,白血病和肾肿瘤细胞已获得AMV - dna。新加入的病毒DNA是单独引起肿瘤变化还是与内源性病毒信息一起引起肿瘤变化还有待阐明。
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Restricted addition of proviral DNA in target tissues of chickens infected with avian myeloblastosis virus.

Proviral DNA is synthesized within an hour after infection of chicken cells with an avian oncornavirus and is integrated into nuclear cellular DNA within a short time. The viral DNA appears to be synthesized as double-stranded molecules of approximately 6 X 10(6) daltons some of which are converted into supercoiled cricles perhaps as a requisite for integration. The endogenous v-DNA in normal chicken cells and both the endogenous and amv v-DNA in leukemic chicken myeloblasts are covalently linked with chromosomal DNA. There is no detectable free DNA either circular or linear present in leukemic cells several weeks after infection. The endogenous v-DNA which is transmitted vertically from parents to offspring is uniformly and stably distributed in all chicken organs. There are about 1-2 copies of endogenous provirus per haploid genome of all normal cells. This DNA is very closely related to RAV-O RNA. After infection with AMV it seems that target cells such as leukemic myeloblasts, RBC and nephroblasts acquire complete copies of AMV DNA. Interestingly, only these target cells can be converted to neoplastic cells in the chicken as well as in vitro. The target cells acquire 1-2 copies of AMV specific DNA per haploid genome in addition to the endogenous v-DNA. All the available evidence shows that leukemic and kidney tumor cells have acquired AMV v-DNA. It remains to be elucidated whether the newly added viral DNA is alone responsible for neoplastic changes or does so in conjunction with endogenous viral information.

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[Bone marrow transplantation in malignant lymphomas?]. Terminal deoxynucleotidyl transferase as a biological marker for human leukemia. [Virus etiology of lymphomas and leukemias in man]. The therapy of acute leukemia in the adult: a progress report. Cellular subclasses in human leukemic hemopoiesis.
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