title: Absence of activating killer immunoglobulin-like receptor genes combined with hepatitis C viral genotype is predictive of hepatocellular carcinoma.
abstract: Killer immunoglobulin-like receptors and their human leukocyte antigen class I ligands have a critical role in natural killer cell response to viral pathogens and tumors. To investigate whether killer immunoglobulin-like receptor genes could influence the chronic course of hepatitis C virus infection and/or progression to hepatocellular carcinoma we retrospectively analyzed a cohort of 228 patients transplanted for hepatitis C virus-induced cirrhotic end stage liver disease, combined or not with hepatocellular carcinoma. We found that patients completely lacking activating killer immunoglobulin-like receptor genes had a high risk of developing hepatocellular carcinoma. Hepatitis C viral genotype and viral load are other risk factors that can influence the course of chronic hepatitis C virus infection. In our study, the risk conferred by hepatitis C viral genotypes was enhanced in patients lacking activating killer immunoglobulin-like receptors. These results point to an important role for activating killer immunoglobulin-like receptors in the control of hepatitis C virus infection and progression to hepatocellular carcinoma. In clinical practice, assessment of killer immunoglobulin-like receptor and hepatitis C viral genotype combinations should allow for more accurate monitoring of patients with chronic hepatitis C virus infection.
authors.affiliation: Centro Regionale Trapianti, Ospedale R. Binaghi - ASL 8, 09126 Cagliari, Italy. Electronic address: roby.litter@gmail.com.
authors.forename: Roberto
authors.initials: R
authors.lastname: Littera
authors.forename: Fausto
authors.initials: F
authors.lastname: Zamboni
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Tondolo
authors.forename: Giovanni
authors.initials: G
authors.lastname: Fantola
authors.forename: Luchino
authors.initials: L
authors.lastname: Chessa
authors.forename: Nicola
authors.initials: N
authors.lastname: Orrù
authors.forename: Marco
authors.initials: M
authors.lastname: Sanna
authors.forename: Donatella
authors.initials: D
authors.lastname: Valentini
authors.forename: Luisella
authors.initials: L
authors.lastname: Cappai
authors.forename: Marina
authors.initials: M
authors.lastname: Mulargia
authors.forename: Giovanni
authors.initials: G
authors.lastname: Caocci
authors.forename: Marcella
authors.initials: M
authors.lastname: Arras
authors.forename: Andrea
authors.initials: A
authors.lastname: Floris
authors.forename: Sandro
authors.initials: S
authors.lastname: Orrù
authors.forename: Giorgio
authors.initials: G
authors.lastname: La Nasa
authors.forename: Carlo
authors.initials: C
authors.lastname: Carcassi
mesh_terms: D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000276:immunology / Q000821:virology*; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006239:Haplotypes; D006526:Hepatitis C / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000821:virology; D006649:Histocompatibility Antigens / Q000235:genetics / Q000276:immunology; D006801:Humans; D008024:Ligands; D008103:Liver Cirrhosis / Q000209:etiology; D008113:Liver Neoplasms / Q000235:genetics* / Q000276:immunology / Q000821:virology*; D008297:Male; D008875:Middle Aged; D054340:Receptors, KIR / Q000235:genetics* / Q000276:immunology; D012189:Retrospective Studies; D019562:Viral Load
chemical_list: D006649:Histocompatibility Antigens; D008024:Ligands; D054340:Receptors, KIR