Mutations in the env gene of friend spleen focus-forming virus overcome Fv-2r-mediated resistance to Friend virus-induced erythroleukemia.

Mutations in the env gene of friend spleen focus-forming virus overcome Fv-2r-mediated resistance to Friend virus-induced erythroleukemia.
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Friend 脾病灶形成病毒的 env 基因突变克服了 Fv-2r 介导的对 Friend 病毒诱导的红白血病的抵抗力。

DOI:
10.1128/jvi.66.6.3652-3660.1992
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发表时间:
1992
影响因子:
5.4
通讯作者:
Geib,RW
Geib,RW
中科院分区:
医学2区
文献类型:
--
作者:
Majumdar,MK;Cho,CL;Fox,MT;Eckner,KL;Kozak,S;Kabat,D;Geib,RW

文献摘要

相似文献

尽管Fv-2 r纯合小鼠对由编码红细胞生成素的病毒或野生型Friend病毒(FV)诱导的白血病具有抗性(M. E. Hoatlin,S. L. Kozak,F. Lilly,A.查克拉博蒂角A. Kozak和D. Kabat,Proc. Natl. Acad. Sci. USA 87:9985-9989,1990),它们对FV的一些变体(R. A. Steeves,E. A. Mirand,A. Bulba和P.J. Trudel,Int. J. Cancer 5:349-356,1970; R. W. Geib,M. B。Seaward,M. L.史蒂文斯,C.- L. Cho和M. Majumdar,Virus Res. 14:161-174,1989)。为了定位参与影响宿主范围的病毒基因,我们克隆并测序了FV的BB 6变体的env基因(Steeves等人,Int. J. Cancer 5:349-356,1970)。与野生型env基因相比,BB 6变体含有159 bp缺失,消除了胞外结构域的近膜部分和58个点突变,导致13个氨基酸的变化。替换的野生型env基因的变体env基因导致在一个重组病毒,产生一个朋友病毒样疾病的Fv-2 r纯合子。我们的研究结果确定了脾病灶形成病毒的env基因参与这种病毒-宿主相互作用的病毒基因。此外,他们认为Fv-2 r基因的产物修饰了脾病灶形成病毒包膜蛋白和促红细胞生成素受体之间的相互作用。
Although Fv-2r homozygous mice are resistant to leukemias induced either by an erythropoietin-encoding virus or by wild-type Friend virus (FV) (M. E. Hoatlin, S. L. Kozak, F. Lilly, A. Chakraborti, C. A. Kozak, and D. Kabat, Proc. Natl. Acad. Sci. USA 87:9985-9989, 1990), they are susceptible to some variants of FV (R. A. Steeves, E. A. Mirand, A. Bulba, and P. J. Trudel, Int. J. Cancer 5:349-356, 1970; R. W. Geib, M. B. Seaward, M. L. Stevens, C.-L. Cho, and M. Majumdar, Virus Res. 14:161-174, 1989). To localize the virus gene involved in influencing the host range, we cloned and sequenced the env gene of the BB6 variant of FV (Steeves et al., Int. J. Cancer 5:349-356, 1970). In comparison with the wild-type env gene, the BB6 variant contains a 159-bp deletion that eliminates the membrane-proximal portion of the extracellular domain and 58 point mutations resulting in 13 amino acid changes. Substitution of the variant env gene for the wild-type env gene resulted in a recombinant virus that produced a Friend virus-like disease in Fv-2r homozygotes. Our results identify the spleen focus-forming virus env gene as the viral gene involved in this virus-host interaction. Additionally, they suggest that the product of the Fv-2r gene modifies the interaction between the spleen focus-forming virus envelope protein and the erythropoietin receptor.