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Hemolytic anemia and erythroleukemia, two distinct pathogenic effects of Friend MuLV: mapping of the effects to different regions of the viral genome.

作者信息

Sitbon M, Sola B, Evans L, Nishio J, Hayes S F, Nathanson K, Garon C F, Chesebro B

出版信息

Cell. 1986 Dec 26;47(6):851-9. doi: 10.1016/0092-8674(86)90800-7.

DOI:10.1016/0092-8674(86)90800-7
PMID:3465451
Abstract

Two different pathogenic effects of the Friend ecotropic murine leukemia virus (F-MuLV) were distinguished by serial examinations of hematocrits and reticulocyte counts of IRW mice inoculated as newborns. F-MuLV induced hemolytic anemia with increased levels of erythropoiesis, which was detectable as early as 13 days of age, whereas blocked erythroid differentiation, associated with erythroleukemia, was apparent only after 30 days of age. Using strains of Friend-MuLV with different virulences, we constructed recombinant viruses that allowed us to map the hemolytic effect and the ability to induce rapid erythroleukemia to different regions of the viral genome. Moreover, the ability of the virus to induce rapid erythroleukemia appeared to be independent of the presence of severe early hemolytic anemia.

摘要

相似文献

1
Hemolytic anemia and erythroleukemia, two distinct pathogenic effects of Friend MuLV: mapping of the effects to different regions of the viral genome.
Cell. 1986 Dec 26;47(6):851-9. doi: 10.1016/0092-8674(86)90800-7.
2
Sequences in the U5-gag-pol region influence early and late pathogenic effects of Friend and Moloney murine leukemia viruses.U5-gag-pol区域的序列影响弗瑞德和莫洛尼鼠白血病病毒的早期和晚期致病效应。
J Virol. 1990 May;64(5):2135-40. doi: 10.1128/JVI.64.5.2135-2140.1990.
3
Identification and mapping of a common proviral integration site Fli-1 in erythroleukemia cells induced by Friend murine leukemia virus.在Friend小鼠白血病病毒诱导的红白血病细胞中常见前病毒整合位点Fli-1的鉴定与定位。
Proc Natl Acad Sci U S A. 1990 Feb;87(4):1332-6. doi: 10.1073/pnas.87.4.1332.
4
A 2.4-kilobase-pair fragment of the Friend murine leukemia virus genome contains the sequences responsible for friend murine leukemia virus-induced erythroleukemia.弗瑞德氏鼠白血病病毒基因组的一个2.4千碱基对片段包含了导致弗瑞德氏鼠白血病病毒诱导性红细胞白血病的序列。
J Virol. 1983 Jun;46(3):718-25. doi: 10.1128/JVI.46.3.718-725.1983.
5
Analysis of two strains of Friend murine leukemia viruses differing in ability to induce early splenomegaly: lack of relationship with generation of recombinant mink cell focus-forming viruses.对两株在诱导早期脾肿大能力上存在差异的弗氏小鼠白血病病毒的分析:与重组貂细胞集落形成病毒产生无关。
J Virol. 1986 Jan;57(1):389-93. doi: 10.1128/JVI.57.1.389-393.1986.
6
Friend murine leukemia virus-induced leukemia is associated with the formation of mink cell focus-inducing viruses and is blocked in mice expressing endogenous mink cell focus-inducing xenotropic viral envelope genes.Friend小鼠白血病病毒诱导的白血病与貂细胞集落诱导病毒的形成有关,并且在表达内源性貂细胞集落诱导异种嗜性病毒包膜基因的小鼠中受到阻断。
J Exp Med. 1981 Sep 1;154(3):907-20. doi: 10.1084/jem.154.3.907.
7
Erythroleukemia induction by replication-competent type C viruses cloned from the anemia- and polycythemia-inducing isolates of Friend leukemia virus.从弗氏白血病病毒的贫血和红细胞增多诱导分离株中克隆出的具有复制能力的C型病毒诱导红白血病
J Exp Med. 1980 Jun 1;151(6):1493-503. doi: 10.1084/jem.151.6.1493.
8
The envelope gene and long terminal repeat sequences contribute to the pathogenic phenotype of helper-independent Friend viruses.包膜基因和长末端重复序列促成了非辅助性弗氏病毒的致病表型。
J Virol. 1984 Sep;51(3):788-94. doi: 10.1128/JVI.51.3.788-794.1984.
9
Susceptibility of BALB/c mice carrying various DBA/2 genes to development of Friend murine leukemia virus-induced erythroleukemia.携带不同DBA/2基因的BALB/c小鼠对Friend小鼠白血病病毒诱导的红白血病发生的易感性。
J Exp Med. 1985 Nov 1;162(5):1579-87. doi: 10.1084/jem.162.5.1579.
10
Sequences responsible for the distinctive hemolytic potentials of Friend and Moloney murine leukemia viruses are dispersed but confined to the psi-gag-PR region.负责弗瑞德和莫洛尼小鼠白血病病毒独特溶血潜能的序列是分散的,但局限于ψ- gag - PR区域。
J Virol. 1993 Sep;67(9):5478-86. doi: 10.1128/JVI.67.9.5478-5486.1993.

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