GENERATION OF MINK CELL FOCUS-FORMING VIRUSES BY FRIEND MURINE LEUKEMIA-VIRUS - RECOMBINATION WITH SPECIFIC ENDOGENOUS PROVIRAL SEQUENCES

GENERATION OF MINK CELL FOCUS-FORMING VIRUSES BY FRIEND MURINE LEUKEMIA-VIRUS - RECOMBINATION WITH SPECIFIC ENDOGENOUS PROVIRAL SEQUENCES
复制标题

DOI:
10.1128/jvi.49.3.772-781.1984
复制
发表时间:
1984-01-01
影响因子:
5.4
通讯作者:
CLOYD, MW
CLOYD, MW
中科院分区:
医学2区
文献类型:
--
作者:
EVANS, LH;CLOYD, MW

文献摘要

被引文献

相似文献

用Friend小鼠白血病病毒接种NFS小鼠,获得了重组水貂细胞聚焦形成病毒(MCF)家族,并利用RNase t1抗性寡核苷酸指纹图谱对其基因组进行了分析。从白血病前期和白血病动物的胸腺和脾脏中获得病毒,并评估其双向性和致癌性。所有分离株均能引起水貂细胞病变灶,但根据其对SC-1(小鼠)或水貂(ATCC - CCL64)细胞的相对感染性可分为2组。一组Friend MCF (F-MCF)(第一组)对SC-1细胞和水貂细胞的感染性大致相同,而第二组(第二组)感染水貂细胞的效率比SC-1细胞高1000至10,000倍。F-MCF的结构分析显示,I组和II组病毒与Friend小鼠白血病病毒的重组具有2个不同但密切相关的内源性NFS前病毒序列。没有发现F-MCF的类型与来源组织或动物疾病状态之间的相关性。在NFS/N或AKR/J小鼠中未发现F-MCF分离株具有致癌性。两组F-MCF均发生了广泛的亲生态序列替换,包括I组F-MCF的大部分gag和env基因,以及II组F-MCF的大部分gag、pol和env基因。所有F-MCF分离株均保留Friend小鼠白血病病毒的3”末端U3区。f -MCF与NFS衍生MCF RNA的比较。akv - 1或NFS。Akv-2小鼠实验表明,F-MCF来源于NFS原病毒序列,与NFS中包含的序列不同。Akv MCF分离株。这一结果表明,与特定的内源性原病毒序列重组产生MCF可能对给定的小鼠白血病病毒具有高度特异性。
A family of recombinant mink cell focus-forming viruses (MCF) was derived by inoculation of NFS mice with a Friend murine leukemia virus, and their genomes were analyzed by RNase T1-resistant oligonucleotide fingerprinting. The viruses were obtained from the thymuses and spleens of preleukemic and leukemic animals and were evaluated for dualtropism and oncogenicity. All these isolates induced cytopathic foci on mink cells but could be classified into 2 groups based on their relative infectivities for SC-1 (mouse) or mink (ATCC CCL64) cells. One group of Friend MCF (F-MCF) (group I) exhibited approximately equal infectivities for SC-1 and mink cells, whereas a second group (group II) infected mink cells 1000-to 10,000-fold more efficiently than SC-1 cells. Structural analyses of the F-MCF revealed that group I and group II viruses correlated with recombinant of Friend murine leukemia virus with 2 distinct, but closely related, endogenous NFS proviral sequences. No correlation was found between the type of F-MCF and the tissue of origin or the disease state of the animal. None of the F-MCF isolates were found to be oncogenic in NFS/N or AKR/J mice. F-MCF of both groups underwent extensive substitution of ecotropic sequences, involving much of the gag and env genes of group I F-MCF and most of the gag, pol and env genes of group II F-MCF. All F-MCF isolates retained the 3'' terminal U3 region of Friend murine leukemia virus. Comparison of the RNA of the F-MCFs with RNA of MCF derived from NFS.Akv-l or NFS.Akv-2 mice indicated that the F-MCF were derived from NFS proviral sequences which are distinct from the sequences contained in NFS.Akv MCF isolates. This result suggested that recombination with particular endogenous proviral sequences to generate MCF may be highly specific for a given murine leukemia virus.