HIV Redirecting Innate Immunity by Vpu Targeting of JAK1

项目摘要/摘要 众所周知，艾滋病毒的发病机制与免疫系统有着千丝万缕的联系。让艾滋病毒促进其 复制和长期感染HIV还必须调节细胞因子信号来操纵免疫 艾滋病病毒存在的微环境。在我们之前的工作中，我们发现HIV编码了附件 能够阻止重要的先天抗病毒细胞因子I型干扰素的作用的基因。类型 I干扰素之所以被命名是因为它们能够干扰病毒的复制，而艾滋病毒已经编码了 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一个 阻断I型干扰素的HIV编码基因可以阻断T细胞中的这种信号，T细胞是感染病毒的主要细胞 爱滋病毒。从长远来看，这项工作对于为更好地了解艾滋病毒如何在人身上自我维持奠定了基础 并避免被先天免疫系统清除。

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.