HEPATITIS-G VIRUS-INFECTION IN CHRONIC DIALYSIS PATIENTS AND KIDNEY-TRANSPLANT RECIPIENTS

Background. The cloning of the hepatitis G virus (HGV), a never RNA vi rus of the Flaviviridae family, has been very recently developed. HGV is known to be parenterally transmitted and has been detected in sever al patients with cryptogenic hepatitis. However, little information ex ists about the epidemiology of HGV infection in renal patients. We stu died 178 chronic dialysis patients and 11 renal transplant individuals to evaluate prevalence, risk factors, and clinical manifestations of HGV infection in this population. Methods. Hepatitis G virus infection has been detected by a modified PCR technology which incorporates dig oxigenin-labelled nucleotides into the amplicon. Primers from the non- coding region and the NS-5 region of HGV are utilized for a single rou nd amplification. Using a streptavidin surface and a biotin-labelled c apture probe, the labelled nucleic acid is bound through the capture p robe to the surface, and the amplified nucleic acid is detected using antibody to digoxigenin. Results. HGV RNA was detected in 6% of chroni c haemodialysis (HD) patients (11/172), 36% of renal transplant recipi ents (4/11), and 17% (1/6) of patients on peritoneal dialysis treatmen t (CAPD). There were no significant differences between HGV positive a nd negative patients on chronic HD treatment with regard to several de mographic, biochemical and virological features. However, the frequenc y of anti-HCV antibody was significantly higher in HGV-positive than H GV-negative patients (9/11 (82%) vs 51/161 (32%), P=0.006). In the who le group of HGV RNA-positive patients, 78% (11/14) had a history of bl ood transfusion requirements, 14/16 (87%) had co-infection with HCV, a nd 1 (6%) had co-infection with HBsAg. There was no significant associ ation between HCV genotypes and HGV RNA positivity. Six (37.5%) of 16 HGV RNA-positive patients showed raised aminotransferase values in ser um. Conclusions. Patients on maintenance dialysis and kidney transplan t recipients are at increased risk of HGV infection; HGV is very frequ ently associated to hepatitis C co-infection, regardless of HCV genoty pe. HGV may be transmitted by blood transfusions but transmission rout es other than transfusion are possible; 37.5% of HGV RNA-positive pati ents showed raised serum aminotransferase levels. Further investigatio ns are necessary to clarify the role of HGV infection in the developme nt of liver disease in this clinical setting.