Abstract
Background and AimTo evaluate in anti-HCV-positive patients the clinical impact of the rs35761398 variant of the CNR2 gene leading to the substitution of Gln (Q) of codon 63 of the cannabinoid receptor 2 (CB2) with Arg (R).Patients and Methods253 consecutive anti-HCV-/HCV-RNA-positive patients were enrolled, of whom 53 were HCV carriers with persistently normal ALT (PNALT group) and 200 had a history of steadily abnormal serum ALT values (abnormal ALT group). All patients were naive for antiviral therapy and were screened for the CNR2 rs35761398 polymorphism by a TaqMan assay.ResultsSubjects in the PNALT group, compared with those in the abnormal ALT group were older (58.5±12 vs. 50.7±12.4 years, p = 0.001), more frequently female (66% vs. 42%, p = 0.003), with lower body massindex (BMI) (24.5±3.1 vs. 26.6±4.6, p = 0.003), and more frequently with HCV genotype 2 (43.1% vs 17.7%, p = 0.0002) and CB2-63 QQ variant (34% vs. 11%, p = 0.0001). Considering all 253 patients, no difference in the demographic, biochemical, or virological data was observed between patients in the different CB2-63 variants. The logistic regression analysis identified CB2-63 QQ, HCV genotype 2, older age and lower BMI as independent predictors of PNALT (p<0.00001).DiscussionThe CB2-63 QQ variant in HCV patients was independently associated with the PNALT status.
Highlights
The Cannabinoid (CB) receptors are seven membrane domain receptors of the G-coupled receptor superfamily that are activated by endogenous or exogenous cannabinoids [1,2]
To confirm our cannabinoid receptor 2 (CB2)-63 data, we considered as two separate cohorts the two series of subjects with hepatitis C virus (HCV) chronic infection included at the two enrolling Liver Units and compared the results obtained
Besides the CB2-63 QQ variant, the multivariate analysis identified another three factors independently associated with the persistently normal ALT (PNALT) status: HCV genotype 2, an older age and a lower body massindex (BMI)
Summary
The Cannabinoid (CB) receptors are seven membrane domain receptors of the G-coupled receptor superfamily that are activated by endogenous (endo) or exogenous (phyto and synthetic) cannabinoids [1,2]. A polymorphism at codon 63 of the Cannabinoid Receptor 2 gene (CNR2) leads to the substitution of glutamine, Gln (Q), with arginine, Arg (R), causing a different polarization state of the protein; the CB2 variants have been demonstrated to affect differently the ability of the CB2 receptor to exert its inhibitory function[5,6]. To evaluate in anti-HCV-positive patients the clinical impact of the rs35761398 variant of the CNR2 gene leading to the substitution of Gln (Q) of codon 63 of the cannabinoid receptor 2 (CB2) with Arg (R)
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