PATHOGENICITY OF SIVMAC239 VARIANTS IN NEONATAL MACAQUES

SIVMAC239 变异体在新生猕猴中的致病性

• 批准号: 7958994
• 负责人: BARBARA K FELBER
• 金额: $ 10.99万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-05-01 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7958994
• 关键词: Attenuated; Biological Models; California; Cells; Computer Retrieval of Information on Scientific Projects Database; Elements; Funding; Grant; Institution; Macaca; Neonatal; Pathogenicity; Primates; Regulation; Research; Research Personnel; Resources; SIV; Source; Subfamily lentivirinae; Type D Retrovirus; United States National Institutes of Health; Variant; Viral; Virus; neonate

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. SIV and all lentiviruses depend on the viral Rev regulation for the nucleo-cytoplasmic export and expression of the RRE-containing mRNAs. We have generated SIV variants that have the essential viral regulatory mechanism replaced by the export elements of the type D retroviruses, CTE, which utilizes a cellular factor hTAP for its transport. Primary cells infected by these SIV variants produce lower amounts of virus having reduced infectivity. The neonate macaque represents a critical and sensitive model system to evaluate the pathogenicity of potentially attenuated SIV variants.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 SIV和所有慢病毒依赖于病毒Rev调节含RRE的mRNA的核质输出和表达。我们已经产生了SIV变体，其具有由D型逆转录病毒CTE的输出元件取代的基本病毒调节机制，CTE利用细胞因子hTAP进行其运输。被这些SIV变体感染的原代细胞产生较少量的具有降低的感染性的病毒。新生猕猴是评价潜在减毒SIV变体致病性的关键和敏感的模型系统。