COXSACKIEVIRUS COMPLEXED WITH THE CELLULAR RECEPTOR, DECAY ACCELERATING FACTOR

柯萨奇病毒与细胞受体、衰变加速因子复合

• 批准号: 8363561
• 负责人: Susan Hafenstein
• 金额: $ 4.51万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-07-01 至 2012-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8363561
• 关键词: Binding; CD55 Antigens; Complex; Coxsackie B Viruses; Coxsackie Viruses; Family; Family Picornaviridae; Funding; Grant; Immunoglobulin G; Infection; Mental Depression; National Center for Research Resources; Pathogenicity; Principal Investigator; Research; Research Infrastructure; Resources; Source; Surface; United States National Institutes of Health; Variant; Virus; Virus Receptors; cost; member; receptor; receptor binding

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Coxsackieviruses are members of the picornavirus family that rely on an interaction with an IgG-like receptor that binds into a depression in the virus surface called the canyon. This interaction causes a conformational change that destabilizes the virus and leads to uncoating. However, some strains of coxsackievirus B group have adapted also to use decay accelerating factor, DAF, as an additional receptor that binds outside of the canyon. These DAF binding variants have altered pathogenicity and preliminary studies show that binding of DAF has become necessary for infection. Preliminary structural studies suggest that when DAF binds CVB3 variants, the virus and the receptor both may undergo conformational changes. We have co-crystallized the virus interacting with the DAF receptor to investigate these changes.

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 柯萨奇病毒是微小核糖核酸病毒家族的成员，它依赖于与一种类似免疫球蛋白的受体的相互作用，这种受体结合到病毒表面被称为峡谷的凹陷中。这种相互作用会导致构象变化，从而破坏病毒的稳定性，并导致脱壳。然而，柯萨奇病毒B组的一些毒株也适应了使用衰变加速因子DAF作为额外的受体，与峡谷外结合。这些DAF结合变异体改变了致病性，初步研究表明，DAF的结合已成为感染所必需的。初步的结构研究表明，当DAF与CVB3变异体结合时，病毒和受体都可能经历构象变化。我们已经将与DAF受体相互作用的病毒共结晶，以研究这些变化。