ANALYSIS OF A FRIEND VIRUS-LIKE DISEASE

朋友病毒样疾病的分析

• 批准号: 3459072
• 负责人: ROY W GEIB
• 金额: $ 6.24万
• 依托单位: INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-07-01 至 1994-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3459072
• 关键词: DNA replication; Friend leukemia; Friend virus; cell differentiation; cell growth regulation; disease /disorder model; erythroid stem cell; erythroleukemia; erythropoiesis; gene expression; genetic manipulation; genetic regulation; genetic strain; laboratory mouse; lactoferrin; membrane activity; molecular cloning; molecular oncology; mutant; neoplasm /cancer genetics; oncogenes; prostaglandin E; receptor; tissue /cell culture; transfection; viral leukemia; viral leukemogenesis; virus envelope; virus genetics; virus infection mechanism; virus protein; virus replication

This project focuses on developing a better understanding of the mechanisms involved in virus-induced leukemogenesis. Specifically this project deals with host-controlled susceptibility to a murine erythroleukemia virus. Fv-2 is a gene in the mouse that modifies susceptibility to a single oncogenic virus, the Spleen Focus-Forming Virus (SFFV). Mice homozygous for the Fv-2r allele (e.g., C57BL/6) are completely resistant to transformation by the spleen focus-forming virus (1). The experiments in this project are devised to characterize the Friend virus-like disease that develops in resistant mice infected with Fv-2rr-adapted strains of Friend Virus. Experiments are proposed that will examine several alternate theories on how the variants acquired the new host range. The studies will examine the possibility that the variants infect progenitor cells at a different stage of differentiation than that infected by the wild-type virus. In addition, the project proposes to clone the Fv-2rr-adapted viruses. The cloned variants will then be analyzed by generating recombinant with wild-type virus and by sequencing the env gene of the variants. The results from this project will enhance our understanding of viral-host interactions, virus-induced transformation, and genetic control of erythroid differentiation.

该项目的重点是更好地了解 病毒诱导白血病发生的机制。 具体来说，该项目涉及宿主控制的易感性 小鼠红白血病病毒 Fv-2是小鼠体内的一种基因， 改变对单一致癌病毒的易感性， 病灶形成病毒（SFFV）。 Fv-2 r纯合子小鼠 等位基因（例如，C57 BL/6）对转化完全抗性 脾病灶形成病毒（1）。 这个实验 该项目旨在描述Friend病毒样疾病的特征， 在感染了Fv-2 rr适应性抗体的小鼠中产生的 朋友病毒的变种 提出的实验将 研究几种不同的理论， 新的主机范围。 这些研究将探讨以下可能性： 所述变体感染处于不同发育阶段的祖细胞， 与野生型病毒感染相比， 在 此外，该项目还建议克隆适应Fv-2 rr的病毒。 然后将通过生成 与野生型病毒重组并通过对env基因测序 的变种。 该项目的成果将提高我们的 了解病毒-宿主相互作用，病毒诱导 转化和红系分化的遗传控制。

项目成果

Rapid capping in alpha-spectrin-deficient MEL cells from mice afflicted with hereditary hemolytic anemia.

• DOI: 10.1083/jcb.125.5.1057
• 发表时间: 1994-06
• 期刊: The Journal of cell biology
• 作者: Dahl SC;Geib RW;Fox MT;Edidin M;Branton D
• 通讯作者: Branton D

RB virus: a strain of Friend virus that produces a 'Friend virus-like' disease in Fv-2rr mice.

RB 病毒：Friend 病毒的一种，可在 Fv-2rr 小鼠中产生“Friend 病毒样”疾病。

• DOI: 10.1016/0168-1702(89)90036-1
• 发表时间: 1989
• 期刊: Virus research
• 影响因子: 5
• 作者: Geib,RW;Seaward,MB;Stevens,ML;Cho,CL;Majumdar,M
• 通讯作者: Majumdar,M

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

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
• 发表时间: 1992
• 期刊: Journal of virology
• 影响因子: 5.4
• 作者: Majumdar,MK;Cho,CL;Fox,MT;Eckner,KL;Kozak,S;Kabat,D;Geib,RW
• 通讯作者: Geib,RW

Deletions in one domain of the Friend virus-encoded membrane glycoprotein overcome host range restrictions for erythroleukemia.

弗兰德病毒编码的膜糖蛋白的一个结构域的缺失克服了红白血病的宿主范围限制。

• DOI: 10.1128/jvi.69.2.856-863.1995
• 发表时间: 1995
• 期刊: Journal of virology.
• 作者: Hoatlin,ME;FerroJr,FE;Geib,RW;Fox,MT;Kozak,SL;Kabat,D
• 通讯作者: Kabat,D