Intracellular innate immune cascades and interferon defenses that control hepatitis C virus.
Hepatitis C virus (HCV) is a global public health problem that mediates a persistent infection in nearly 200 million people. HCV is efficient in establishing chronicity due in part to the inefficiency of the host immune system in controlling and counteracting HCV-mediated evasion strategies. HCV persistence is linked to the ability of the virus to suppress the RIG-I pathway and interferon production from infected hepatocytes, thus evading innate immune defenses within the infected cell. This review describes the virus and host processes that regulate the RIG-I pathway during HCV infection. An understanding of these HCV-host interactions could lead to more effective therapies for HCV designed to reactivate the host immune response following HCV infection.
Horner
Stacy M
SM
Department of Immunology, University of Washington School of Medicine, Seattle, Washington 98195, USA.
Gale
Michael
M
D000818:Animals; D004791:Enzyme Inhibitors / Q000276:immunology / Q000378:metabolism*; D005786:Gene Expression Regulation; D016174:Hepacivirus / Q000472:pathogenicity / Q000502:physiology*; D006526:Hepatitis C / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000276:immunology*; D042541:Intracellular Space / Q000276:immunology / Q000378:metabolism; D018168:Receptors, Retinoic Acid / Q000037:antagonists & inhibitors / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D014764:Viral Proteins / Q000276:immunology / Q000378:metabolism*; D014774:Virulence
D004791:Enzyme Inhibitors; C437968:PLAAT4 protein, human; D018168:Receptors, Retinoic Acid; D014764:Viral Proteins; D007372:Interferons