title: [Immune dysregulation mediated by hepatitis C virus infection].
abstract: Hepatitis C virus, which is non-cytopathic, establishes persistent infection in majority of patients after acute infection, causing various degrees of clinical liver disease. To escape and survive, hepatitis C virus may take ingenious strategies. Hepatitis C virus gene products interact host proteins to evade host immune responses in addition to the appearance of quasispecies. Against hepatitis C virus infection, host may avoid extensive tissue damage by inducing the activity of regulatory T cells. Insights into this mechanism of immune regulation may help to future development of novel therapies against hepatitis C virus.
authors.affiliation: School of Health, Faculty of Medicine, Tohoku University, 2-1, Seiryoumachi, aobaku, Sendaishi 980-8575, Japan. kobakoju@mail.tains.tohoku.ac.jp
authors.forename: Koju
authors.initials: K
authors.lastname: Kobayashi
mesh_terms: D000818:Animals; D003713:Dendritic Cells / Q000276:immunology; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology*; D006526:Hepatitis C / Q000276:immunology*; D006801:Humans; D007157:Immunologic Surveillance; D007372:Interferons; D007694:Killer Cells, Natural / Q000276:immunology; D008562:Membrane Glycoproteins / Q000276:immunology; D011951:Receptors, Complement / Q000276:immunology; D015398:Signal Transduction; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D014764:Viral Proteins / Q000276:immunology
chemical_list: D008562:Membrane Glycoproteins; D011951:Receptors, Complement; D014764:Viral Proteins; C032402:complement 1q receptor; D007372:Interferons