HIV Redirecting Innate Immunity by Vpu Targeting of JAK1

HIV 通过 Vpu 靶向 JAK1 重定向先天免疫

基本信息

批准号：
10619889
负责人：
DAVID JESSE SANCHEZ
金额：
$ 7.15万
依托单位：
WESTERN UNIVERSITY OF HEALTH SCIENCES
依托单位国家：
美国
项目类别：
财政年份：
2023
资助国家：
美国
起止时间：
2023-06-20 至 2025-05-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10619889
关键词：
Amino Acid Motifs Biochemical CD4 Positive T Lymphocytes Cell physiology Cells Cellular Immunity Cellular biology Cytokine Receptors Cytokine Signaling Data Dendritic Cells Detection Genes Goals HIV HIV Infections Immune response Immune system Immunity Infection Innate Immune Response Innate Immune System Interferon Type I Interferon Type II Interferons JAK1 gene Link Lysosomes Maps Mediating Methods Mutation Analysis Names Natural Immunity Outcome Pathogenesis Patients Persons Phenotype Phosphorylation Production Proteins Refractory Research Project Grants STAT1 gene Serum Signal Transduction System T-Lymphocyte Techniques Tertiary Protein Structure Ubiquitination Viral Virus Virus Diseases Virus Replication Work adaptive immunity antiviral immunity arm cellular targeting cytokine domain mapping experience immune clearance insight multicatalytic endopeptidase complex response tumor-immune system interactions vpu Protein

项目摘要

Project Summary/Abstract It is well known that the pathogenesis of HIV is intricately linked to the immune system. For HIV to promote its replication and long-term infection HIV must also modulate cytokine signaling to manipulate the immune microenvironment HIV is existing in. In our previous work we have found that HIV has encoded accessory genes that are able to block the action of the important innate antiviral cytokine named Type I Interferon. Type I Interferons were named for their ability to interfere with the replication of viruses and HIV has encoded multiple ways to block this cytokine. The overall goal of this R03 application is to determine how one of the HIV-encoded genes that blocks Type I Interferon can block this signaling in T cells, the major cell infected by HIV. Long term, this work is critical to set the stage to better understand how HIV sustains itself in a person and avoids elimination by the innate immune system.

项目概要/摘要众所周知，艾滋病毒的发病机制与免疫系统有着复杂的联系。对于艾滋病毒促进其复制和长期感染 HIV 还必须调节细胞因子信号传导来操纵免疫系统 HIV存在的微环境。在我们之前的工作中，我们发现HIV编码了辅助病毒能够阻断重要的先天抗病毒细胞因子（称为 I 型干扰素）作用的基因。类型 I 干扰素因其干扰病毒复制的能力而得名，而 HIV 已编码有多种方法可以阻断这种细胞因子。此 R03 应用程序的总体目标是确定其中之一如何阻断 I 型干扰素的 HIV 编码基因可以阻断 T 细胞（感染艾滋病病毒的主要细胞）中的这种信号传导。艾滋病病毒。从长远来看，这项工作对于更好地了解艾滋病毒如何在人体内持续存在至关重要并避免被先天免疫系统消除。