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MECHANISMS OF PATHOGENESIS AND RECOVERY FROM FRIEND MURINE LEUKEMIA VIRUS

MECHANISMS OF PATHOGENESIS AND RECOVERY FROM FRIEND MURINE LEUKEMIA VIRUS
鼠友白血病病毒的发病机制和恢复机制
批准号:
2566698
负责人:
B CHESEBRO
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
Friend病毒(FV)是两种小鼠逆转录病毒的复合体, 在许多品系的成年小鼠中发生快速红白血病。今年我们 实验集中在某些病毒基因对两个 与辅助病毒成分有关的病毒发病机制方面 复杂的。Friend MuLV与Moloney MuLV作为辅助治疗的比较 FV复合体的SFFV组件有缺陷,这表明莫洛尼是 远不如Friend作为体内辅助病毒。随后的实验 已经使用嵌合感染性病毒来确定 朋友病毒是需要高效率作为帮手的.结果 表明gag基因的两个部分参与了该效应, 不过,有关机制仍在调查中。 来自上述研究的嵌合Friend/Moloney病毒也用于 确定不同病毒env基因对相互作用的影响 FV复合物与免疫系统,特别是主要 组织相容性复合体基因。辅助病毒与莫洛尼囊膜病毒 和AKV env目前正在实验中。 小鼠逆转录病毒env基因变异在诱导小鼠白血病中的作用 神经发病机制也正在使用Friend的98 D菌株进行研究 MCF多嗜性逆转录病毒。结果表明,两种不同的 env基因的区域可产生神经毒性表型。这些 这些发现可能与艾滋病毒引起的脑部疾病有一些相似之处, 被感染的人类
英文摘要
Friend virus (FV) is a complex of two mouse retroviruses which induce rapid erythroleukemia in many strains of adult mice. This year our experiments have focussed on the influence of certain viral genes on two aspects of viral pathogenesis related to the helper virus component of the complex. Comparison of Friend MuLV versus Moloney MuLV as helpers for the defective SFFV component of the FV complex revealed that Moloney was far inferior to Friend as a helper virus in vivo. Subsequent experiments have used chimeric infectious viruses to determine which regions of Friend virus are required for high efficiency as a helper. The results indicate that two portions of the gag gene are involved in this effect, however the mechanism is still under investigation. Chimeric Friend/Moloney viruses from the above study were also used to determine the influence of different viral env genes on the interaction of FV complex with the immune system and in particular the major histocompatibility complex genes.Helper viruses with both the Moloney env and the AKV env are currently under experimentation. The role of mouse retroviral env gene variation in induction of neuropathogenesis is also being studied using the 98D strain of Friend MCF polytropic retrovirus. The results indicate that two different regions of the env gene can give a neurovirulent phenotype. These findings may have some similarities to brain disease induced by HIV in infected humans.
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