Absence of activating killer immunoglobulin-like receptor genes combined with hepatitis C viral genotype is predictive of hepatocellular carcinoma

CHESSA, LUCHINO
Writing - Original Draft Preparation
;
CAOCCI, GIOVANNI
Writing - Review & Editing
;
FLORIS, ANDREA;ORRU, SANDRO;LA NASA, GIORGIO
Penultimate
Writing - Review & Editing
;
CARCASSI, CARLO
Last
Writing - Original Draft Preparation
2013-01-01

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.
2013
Inglese
74
10
1288
1294
7
Esperti anonimi
scientifica
no
Littera, R; Zamboni, F; Tondolo, V; Fantola, G; Chessa, Luchino; Orrù, N; Sanna, M; Valentini, D; Cappai, L; Mulargia, M; Caocci, Giovanni; Arras, M; ...espandi
1.1 Articolo in rivista
info:eu-repo/semantics/article
1 Contributo su Rivista::1.1 Articolo in rivista
262
16
reserved
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