Intrahepatic hepatitis C virus replication is increased in patients with regular alcohol consumption

Aims. To assess clinical significance of liver hepatitis C virus PNA levels and their relationship with epidemiological, biochemical and histological factors. Methods. A total of 50 patients (mean age 35.5 +/-7 years) with biopsy-prov en chronic hepatitis C infection were recruited. Risk factors were drug abu se [n=21], transfusion [n=16], other parental routes (n=B; surgery=3, tatto oing=5], and idiopathic [n=5]. Duration of infection was 16 +/-9 years. All patients showed abnormal alanine aminotransferase levels and positive seru m hepatitis C virus RNA. Hepatitis C virus genotype was assessed by Inno-Li pa. Liver biopsy was performed for histology and for hepatitis C virus PNA quantification by Amplicor-HCV-Monitor Daily alcohol consumption was record ed on two occasions by anamnesis. Inflammation grade was mild [n=31] or sev ere [n= 19]. Fibrosis was early stage [n=42] or advanced [n=B]. Results. Mean hepatitis C virus PNA levels were 9.4x10(5)+/-1.5x10(6) copie s/mug of total PNA in liver tissue, and 9.1x10(6 +/-)1.3x10(6) copies/ml in serum. Viral load in liver was positively correlated with that in serum [r =0.51, p <0.001] and there was a significant relationship between daily alc ohol consumption and intrahepatic hepatitis C virus burden [r=0.53; p<0.001 ]. Patients infected with genotype 3a showed lower intrahepatic hepatitis C virus load than patients infected with genotype 1b; albeit without reachin g statistical significance [0.49x10(6)<plus/minus>0.89x10(6) vs 1.44x10(6)/-1.9x10(6) copies/mug of total PNA; p=NS]. No relationships were observed between liver viral burden and age, risk factor status, duration of infecti on, ferritin and alanine aminotransferase levels or with grading and stagin g. Conclusions. Hepatitis C virus load in serum is a mirror of intrahepatic he patitis C virus levels. Chronic alcohol consumption enhances intrahepatic h epatitis C virus concentration.