MINORITY PREDOCTORAL FELLOWSHIP PROGRAM

少数族裔博士前奖学金计划

• 批准号: 6590711
• 负责人: BRUNO SAINZ
• 金额: $ 2.54万
• 依托单位: TULANE UNIVERSITY OF LOUISIANA
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-05-30 至 2006-05-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6590711
• 关键词: cell line; endoribonucleases; gene complementation; gene expression; gene induction /repression; genetic translation; herpes simplex virus 1; host organism interaction; immediate early protein; interferon beta; interferon gamma; latent virus infection; northern blottings; peripheral nervous system; polymerase chain reaction; predoctoral investigator; protein kinase; protein structure function; transmission electron microscopy; virus DNA; virus assembly; virus genetics; virus infection mechanism; virus protein; western blottings

DESCRIPTION (provided by applicant): The process by which herpes simplex virus type 1 (HSV-1) establishes latency in neurons of the peripheral nervous system is poorly defined. Although considerable evidence suggests that CD8 + T cells and IFN-gamma contribute to the establishment of latency, direct evidence to support this hypothesis is lacking. In particular, a limiting factor in elucidating the mechanism(s) by which IFN-gamma could potentially inhibit viral replication is that IFN-gamma alone only marginally inhibits HSV-1 replication in vitro. Consequently, it is difficult to determine how IFN-gamma contributes to the establishment of viral latency. We have identified an unexpected event by which IFN-gamma can function m concert with IFN-beta to potently inhibit HSV-1 replication both in vitro and in vivo. The goal of the studies proposed herein is to elucidate the mechanism(s) by which IFN-beta and IFN-gamma inhibit HSV-1 replication and to identify the cellular factors that are involved in this process.

描述（由申请人提供）： 单纯疱疹病毒1型（HSV-1）在周围神经系统的神经元中建立潜伏期的过程很差。 尽管大量证据表明，CD8 + T细胞和IFN-Gamma有助于建立潜伏期，但缺乏支持该假设的直接证据。特别是，阐明IFN-GAMMA可能抑制病毒复制的机制的限制因素是，仅IFN-GAMMA仅在体外仅略微抑制HSV-1复制。因此，很难确定IFN-gamma如何促进病毒潜伏期的建立。我们已经确定了一个意想不到的事件，IFN-gamma可以与IFN-beta进行音乐会，从而有效抑制体外和体内的HSV-1复制。本文提出的研究的目的是阐明IFN-BETA和IFN-GAMMA抑制HSV-1复制的机制，并确定此过程中涉及的细胞因子。