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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
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中文摘要
翻译
Friend病毒(Friend Virus,FV)是由两种可诱导小鼠感染的逆转录病毒组成的复合体。 在许多品系的成年小鼠中出现快速红白血病。今年我们的 实验的重点是某些病毒基因对两种病毒的影响 与辅助性病毒成分相关的病毒致病机制 这个建筑群。Friend MuLV和Moloney MuLV作为帮手的比较 FV复合体的有缺陷的SFFV成分表明Moloney是 作为活体内的辅助病毒,远远不如Friend。随后的实验 已经使用嵌合感染病毒来确定 朋友病毒是作为帮手的高效率所必需的。结果是 表明Gag基因的两个部分参与了这一效应, 然而,这一机制仍在调查中。 来自上述研究的嵌合Friend/Moloney病毒也被用于 确定不同的病毒包膜基因对相互作用的影响 与免疫系统的FV复合体,特别是主要的 组织相容性复合体基因.同时具有Moloney环境的辅助病毒 和AKV env目前正在进行试验。 小鼠逆转录病毒env基因变异在诱导猪瘟病毒感染中的作用 神经发病机制也正在使用Friend的98d株进行研究。 MCF多嗜性逆转录病毒。结果表明,两种不同的 Env基因的区域可以给出神经毒力的表型。这些 研究结果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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