Virus-Host interactions regulating HIV-1 replication in T cells. (360G-Wellcome-108079_Z_15_Z)

Human Immunodeficiency Virus Type-1 (HIV-1), the cause of the global AIDS pandemic, predominantly infects cells of the immune system called CD4+ T cells. In order to do this successfully, HIV-1 must navigate a complex environment by hijacking the essential cellular machinery that it needs to replicate and spread, while at the same time avoiding host defense mechanisms. Understanding exactly how HIV-1 does this and how this contributes to AIDS is the aim of this project. An important property of immune cells, including T cells, is their ability to rapidly respond to their environment by relaying signals to convey information. This is essential for the immune system to function normally. My laboratory has made new discoveries about what signals HIV-1 triggers in T cells that likely contribute to successful infection and spread. We will now perform experiments to understand exactly how these cellular molecules work; how HIV-1 hijacks them to its own advantage; and how this contributes to T cell death and disease. From our studies we aim to identify cellular and viral factors that maybe targeted by new drugs to block HIV-1 replication, eradicate the virus and stop the progression to AIDS.