权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Varicella-Zoster Virus: T Cell/Skin Tropisms & Immunity

水痘带状疱疹病毒：T 细胞/皮肤趋向性

基本信息

批准号：
9968744
负责人：
Stefan Lyne Oliver
金额：
$ 39.42万
依托单位：
STANFORD UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
1994
资助国家：
美国
起止时间：
1994-08-01 至 2024-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9968744
关键词：
Address Adult Amino Acids Antibodies Antiviral Agents Axonal Transport Cell Surface Receptors Cell Survival Cell fusion Cells Chickenpox Chinese Hamster Ovary Cell Complement Complement Activation Complement Membrane Attack Complex Complex Cytolysis Elements Equilibrium Event Exanthema Gel Genes Glycoproteins Grant HSV glycoprotein C Hematogenous Herpes zoster disease Herpesviridae Herpesvirus 1 Herpesvirus Type 3 Human Immune response Immunity Immunoprecipitation In Vitro Incubated Infection Inflammasome Instruction Knowledge Libraries Life Cycle Stages Maps Mass Spectrum Analysis Mediating Membrane Methods Molecular Mutation Neurons PI3 gene Pathogenesis Phosphorylation Phosphotransferases Platelet-Derived Growth Factor Receptor Primary Infection Production Proteins Receptor Cell Recovery Regulation Reporting Research Respiratory System Role SCID Mice Second Messenger Systems Sensory Sensory Ganglia Sepharose Serum Severe Combined Immunodeficiency Signal Pathway Signal Transduction Site Skin T-Lymphocyte Testing Tissues Tonsil Tropism Viral Viral Genes Viral Pathogenesis Viral Proteins Virion Virus Virus Activation Virus Diseases Virus Replication Work base cancer cell cancer type complement system defined contribution design experimental study genetic regulatory protein innovation insight knock-down mouse model pathogenic virus programs promoter protein activation protein kinase R receptor receptor binding recombinant virus skin xenograft virus tropism

项目摘要

Varicella-zoster virus is an alpha-herpesvirus that causes varicella and zoster. Infection of T cells allows VZV transfer from the respiratory tract to skin and the typical herpes zoster rash results from axonal transport after VZV reactivation in neurons. Our research program investigates the mechanisms of VZV take-over of its target cells, focusing on infection of primary human tonsil T cells and adult skin xenografts in the severe combined immunodeficiency (SCIO) mouse model. We plan to pursue our longstanding objective to understand of VZV pathogenesis in new directions that are designed to determine the role of activation of protein kinase R in VZV infection, the effects of complement as an innate defense against VZV infection of tonsil T cells and VZV countermeasures, and glycoprotein-mediated mechanisms of VZV entry into T cells. This work is expected to provide new knowledge about the takeover of host cell signaling pathways by VZV to support its replication, the regulation of VZV pathogenesis by innate host responses and how VZV overcomes these barriers, and the functions of VZV glycoproteins during infection of differentiated human cells, all of which are critical for VZV infection of the human host. RELEVANCE (See instructions):

水痘带状疱疹病毒是一种引起水痘和带状疱疹的α -疱疹病毒。T细胞感染允许