HIV Redirecting Innate Immunity by Vpu Targeting of JAK1

项目总结/摘要 众所周知，艾滋病毒的发病机制与免疫系统密切相关。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以操纵免疫系统， 艾滋病病毒存在的微环境。在我们以前的工作中，我们发现艾滋病毒编码了附件， 这些基因能够阻断重要的先天性抗病毒细胞因子I型干扰素的作用。类型 干扰素因其干扰病毒复制的能力而命名，HIV编码了 多种方法来阻断这种细胞因子。此R 03应用程序的总体目标是确定 阻断I型干扰素的HIV编码基因可以阻断T细胞中的这种信号传导，T细胞是受感染的主要细胞。 艾滋病。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自我维持至关重要 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.