Ebola Virology

埃博拉病毒学

• 批准号: 9161770
• 负责人: NANCY J SULLIVAN
• 金额: $ 49.42万
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/9161770
• 关键词: Antiviral Agents; Binding; Biology; Cell Surface Receptors; Cell fusion; Cell membrane; Cells; Disease; Ebola virus; Event; Genome; Glycoproteins; Goals; Immune response; Laboratories; Life Cycle Stages; Mediating; Molecular; Open Reading Frames; Property; RNA Viruses; Viral; Virus; Virus Diseases; Virus Replication; cell type; interest; virology; virus host interaction; virus pathogenesis

This study aims to better understand the mechanisms by which Ebola virus infects cells and causes disease. To better understand the mechanisms by which Ebola virus infects cells and causes disease. Our laboratory is interested the basic biology underlying Ebola virus pathogenesis, virus-host interactions, and inhibition of virus replication. Ebola virus is a non-segmented negative strand RNA virus with a simple genome containing seven open reading frames. The virus replication cycle begins with binding of the envelope glycoprotein, GP, to a putative cell surface receptor(s) and entry into the host cell by fusion of viral and cell membranes. Strategies to interrupt the virus life cycle can be targeted to these early entry events or to later steps in the replication cycle. Our hypothesis is that molecular events underlying Ebola GP interactions within the host contribute to preferential targeting of Ebola virus infection to specific cell types, mediate pathogenic properties of the virus, and influence immune responses generated against the virus. Our goal with these studies is to identify points in the Ebola virus replication cycle that are vulnerable antiviral and neutralization targets. We are approaching this goal with several aims, each focusing on a particular aspect of GP function.

这项研究旨在更好地了解埃博拉病毒感染细胞并引起疾病的机制。更好地了解埃博拉病毒感染细胞并引起疾病的机制。我们的实验室对埃博拉病毒发病机理，病毒宿主相互作用和抑制病毒复制感兴趣。埃博拉病毒是一种非细分负链RNA病毒，其简单基因组包含七个开放式阅读框。病毒复制周期始于包膜糖蛋白GP与假定细胞表面受体的结合，并通过融合病毒和细胞膜的融合进入宿主细胞。中断病毒生命周期的策略可以针对这些早期进入事件，也可以针对复制周期中的以后步骤。 我们的假设是，宿主中埃博拉GP相互作用的分子事件有助于将埃博拉病毒感染靶向特定细胞类型，介导病毒的致病性质并影响针对病毒的免疫反应。这些研究的目标是确定埃博拉病毒复制周期中易受攻击的抗病毒和中和靶标的点。我们正在以几个目标来实现这一目标，每个目标都集中在GP功能的特定方面。