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Hepatitis C Virus Protein NS5A Blocks Sendai Virus-Mediated Nuclear Translocation of the Transcription Factor NF-kB
Richards, Josey
Richards, Josey
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Date
2016
Additional date(s)
2016-05-19
Abstract
Hepatitis C Virus (HCV) is an enveloped, positive-stranded RNA virus that infects liver cells, leading to liver damage and cancer. HCV infection causes Hepatitis C in an estimated 170 million people worldwide. Currently, there are treatment options for Hepatitis C but treatment is not 100% effective and instigates severe side effects. Further research into the life cycle and pathogenesis is necessary to develop better treatments and potentially a vaccine. HCV evades the host cell immune response through multiple mechanisms, one of which is through the inhibition of interferon-B expression by NS5A: K2040. When a cell detects viral infection, three transcription factors translocate from the cytoplasm into the nucleus to bind to the IFN-beta promoter: ATF-2, IRF-3, and NF-kB. Binding to the promoter turns on the IFN-beta gene and leads to IFNB expression. Therefore, HCV NS5A: K2040 could potentially prevent IFN-beta expression through inhibiting the translocation of one or more of the transcription factors. Using immunofluorescence analysis in HeLa cells, the cellular location of transcription factors before and after viral infection was examined. The results indicated that NS5A does not block the translocation of ATF-2 or IRF-3. However, NS5A prevented translocation of NF-KB indicating that NS5A attenuates IFN-beta expression through inhibition of the translocation of NF-KB.
Contents
Subject
Hepatitis C Virus
NS5A
Innate Immunity
Antiviral Response
Interferon-Beta
NF-kB
ATF-2
IRF-3
TNF-alpha
NS5A
Innate Immunity
Antiviral Response
Interferon-Beta
NF-kB
ATF-2
IRF-3
TNF-alpha
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Research Projects
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Department
Biology