HERPES SIMPLEX VIRUS FC RECEPTOR

单纯疱疹病毒 FC 受体

• 批准号: 2661091
• 负责人: Harvey Michael Friedman
• 金额: $ 20.43万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-07-01 至 1998-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2661091
• 关键词: antibody receptor; antigen antibody reaction; complement; disease /disorder model; enzyme linked immunosorbent assay; gel electrophoresis; gene mutation; genetic manipulation; glycoproteins; herpes simplex virus 1; herpes simplex virus 2; human subject; immunofluorescence technique; immunoglobulin G; immunoglobulin structure; laboratory mouse; molecular cloning; passive immunization; pathologic process; receptor binding; transfection; virus protein; virus replication

DESCRIPTION: This proposal examines the role of the herpes simplex virus (HSV) IgG Fc receptor (FcR) in immune evasion. The goals of the proposal are to: (1) demonstrate the biologic significance of the HSV-1 FcR in vivo. This will be done using FcR mutant and rescued viruses. (2) Define the functional domains involved in HSV-1 and HSV-2 FcR activity. Mapping studies will explore the role of HSV-1 gI and HSV-2 gE and gI in FcR-mediated immune evasion. (3) Block HSV FcR-mediated immune evasion. The investigators propose a series of vaccine candidates designed to induce antibodies that will block FcR activity and hopefully improve HSV vaccine efficacy.

描述：该提案检查了疱疹单纯性病毒的作用 （HSV）IgG FC受体（FCR）在免疫逃避中。提案的目标 为：（1）证明了体内HSV-1 FCR的生物学意义。 这将使用FCR突变体和救出病毒进行。 （2）定义 与HSV-1和HSV-2 FCR活性有关的功能域。映射 研究将探讨HSV-1 GI和HSV-2 GE和GI在 FCR介导的免疫逃避。 （3）阻断HSV FCR介导的免疫逃避。 研究人员提出了一系列旨在诱导的疫苗候选者 可以阻止FCR活性并希望改善HSV疫苗的抗体 功效。