PATHOGENICITY OF SIVMAC239 VARIANTS IN NEONATAL MACAQUES

SIVMAC239 变异体在新生猕猴中的致病性

• 批准号: 7349647
• 负责人: BARBARA K FELBER
• 金额: $ 15.67万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7349647
• 关键词: PATHOGENICITY; SIVMAC239; VARIANTS; NEONATAL; MACAQUES

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. Objective: 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.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。目的：SIV和所有慢病毒依赖于核总质出口的病毒REV调节和含RRE的mRNA的表达。我们已经产生了具有必需病毒调节机制的SIV变体，被D型逆转录病毒CTE的出口元件取代，该逆转录病毒CTE的输出元素利用细胞因子HTAP进行运输。被这些SIV变体感染的原代细胞会产生较低量的感染性病毒。新生儿猕猴代表了一个关键而敏感的模型系统，用于评估潜在减弱的SIV变体的致病性。