Evasion of intracellular host defence by hepatitis C virus.
Viral infection of mammalian cells rapidly triggers intracellular signalling events leading to interferon alpha/beta production and a cellular antiviral state. This 'host response' is our first line of immune defence against infection as it imposes several barriers to viral replication and spread. Hepatitis C virus (HCV) evades the host response through a complex combination of processes that include signalling interference, effector modulation and continual viral genetic variation. These evasion strategies support persistent infection and the spread of HCV. Defining the molecular mechanisms by which HCV regulates the host response is of crucial importance and may reveal targets for novel therapeutic strategies.
Gale
Michael
M
Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9048, USA michael.gale@utsouthwestern.edu
Foy
Eileen M
EM
D000818:Animals; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D006526:Hepatitis C / Q000276:immunology* / Q000821:virology*; D006790:Host-Parasite Interactions; D006801:Humans; D007372:Interferons / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction
D007372:Interferons