| Abstract | Hepatitis C Virus (HCV) infects liver cells, and is capable of setting up a chronic infection. HCV is a single-stranded, enveloped virus that has a genome that codes for 10 structural and non-structural proteins. Some of these proteins serve dual functions in the virus life cycle and in evading the host immune system. One of the antiviral pathways targeted by the HCV is the interferon-beta (IFN-b) production pathway of the innate immune system. Production of IFN-beta alerts an infected cell and the surrounding cells to the presence of a pathogen and results in the production of antiviral proteins and the establishment of an antiviral state in the cell. To be effective, transcription of IFN-beta requires three transcription factors: IRF-3, NF-KB, and ATF-2. The focus of our research is to understand how an HCV non-structural protein NS5A, affects the activation of the IFN-beta gene and the production of the interferon protein. Studies that a mutation in NS5A can inhibit activation of IFN-beta gene. It is our hypothesis that HCV Non-structural protein 5A inhibits the expression of IFN-beta by blocking nuclear localization of the transcription factors required to transcribe the Interferon-beta gene. To test this hypothesis, 293 HEK cells cells expressing NS5A were treated with Sendai virus. Following infection cells were fixed and stained with antibodies against IRF-3 and NS5A. Fluorescence microscopy was used to reveal the location of the different proteins post infection and to determine whether nuclear translocation was affected by NS5A. |
