Hepatitis G virus RNA and hepatitis G virus antibodies in renal transplant recipients: prevalence and risk factors.

BACKGROUND Hepatitis G virus (HGV/GBV-C) RNA indicating current infection has been frequently isolated from the sera of transplant recipients and other multitransfused individuals. Lifetime exposure to the virus, however, is unknown. We carried out a study to determine the prevalence and risk factors of HGV antibodies and of HGV RNA among renal transplant recipients, and to investigate possible associations between HGV RNA and immunosuppressive treatment. METHODS HGV RNA was detected by reverse transcriptase-polymerase chain reaction, and HGV antibodies (anti-E2) by a newly developed immunoassay. To assess risk factors for HGV exposure, univariate and multivariate analysis was performed. RESULTS Of the 221 patients, 14% were HGV RNA positive and 40% had HGV antibodies. Both HGV RNA and anti-HGV were present in only two individuals. Thus, the overall HGV exposure prevalence was 53%. It increased significantly with the number of blood transfusions. In logistic regression, the adjusted HGV exposure prevalence odds ratio was 5.7 (95% confidence interval [CI]: 2.2-15) among patients with > or =10 transfusions (baseline: no transfusions). Other independent risk factors were a longer duration of hemodialysis and a longer time interval since transplantation. HGV viremia was not associated with the type of immunosuppressive treatment. Alanine aminotransferase levels were not significantly increased among HGV RNA-positive patients. CONCLUSIONS Much higher proportions of renal transplant recipients were exposed to HGV than is suggested by HGV RNA detection alone. The majority of infected individuals apparently eliminate the virus over time. Contaminated blood transfusions have to be regarded as a main risk factor for HGV infection.

[1]  K. Stark,et al.  Detection of antibodies to a putative hepatitis G virus envelope protein , 1997, The Lancet.

[2]  M. Piatak,et al.  Hepatitis G virus infection: clinical characteristics and response to interferon , 1997, Journal of viral hepatitis.

[3]  P. Simmonds,et al.  The clinical significance of the detection of hepatitis GBV‐C RNA in the serum of patients with fulminant, presumed viral, hepatitis , 1997, Journal of viral hepatitis.

[4]  M. Manns,et al.  Association between fulminant hepatic failure and a strain of GBV virus C , 1996, The Lancet.

[5]  K. Stark,et al.  Detection of the hepatitis G virus genome among injecting drug users, homosexual and bisexual men, and blood donors. , 1996, The Journal of infectious diseases.

[6]  P. Simmonds,et al.  Infection with hepatitis G virus among recipients of plasma products , 1996, The Lancet.

[7]  T. Pilot‐Matias,et al.  Expression of the GB virus C E2 glycoprotein using the Semliki Forest virus vector system and its utility as a serologic marker. , 1996, Virology.

[8]  S. Schmolke,et al.  Reverse transcription-PCR detection of hepatitis G virus , 1996, Journal of Clinical Microbiology.

[9]  E. Silini,et al.  Hepatitis G virus and post-transplantation hepatitis. , 1996, The New England journal of medicine.

[10]  T. Berg,et al.  GB virus C infection in patients with chronic hepatitis B and C before and after liver transplantation. , 1996, Transplantation.

[11]  M. Mizokami,et al.  Hepatitis G virus in immunosuppressed paediatric allograft recipients , 1996, The Lancet.

[12]  J. Rosenblatt,et al.  Prevalence studies of GB Virus‐C infection using reverse transcriptase‐polymerase chain reaction , 1996, Journal of medical virology.

[13]  S. Myint,et al.  Aplastic anaemia after HGV infection , 1996, The Lancet.

[14]  H. Okamoto,et al.  Infection with GB virus C (GBV‐C) in patients with chronic liver disease or on maintenance hemodialysis in Indonesia , 1996, Journal of Medical Virology.

[15]  D. Milligan,et al.  Hepatitis G virus in long-term survivors of haematological malignancy , 1996, The Lancet.

[16]  K. Masuko,et al.  Infection with hepatitis GB virus C in patients on maintenance hemodialysis. , 1996, New England Journal of Medicine.

[17]  H. Alter The cloning and clinical implications of HGV and HGBV-C. , 1996, The New England journal of medicine.

[18]  R. Charrel,et al.  Hepatitis GB virus C in patients on hemodialysis. , 1996, The New England journal of medicine.

[19]  H. Margolis,et al.  Molecular Cloning and Disease Association of Hepatitis G Virus: A Transfusion-Transmissible Agent , 1996, Science.

[20]  Ding‐Shinn Chen,et al.  GBV-C in the aetiology of fulminant hepatitis , 1996, The Lancet.

[21]  T. Pilot‐Matias,et al.  Sequence and genomic organization of GBV‐C: A novel member of the flaviviridae associated with human non‐A‐E hepatitis , 1996, Journal of medical virology.

[22]  S. Mishiro,et al.  Detection of the GBV-C hepatitis virus genome in serum from patients with fulminant hepatitis of unknown aetiology , 1995, The Lancet.

[23]  T. Pilot‐Matias,et al.  Isolation of novel virus-like sequences associated with human hepatitis , 1995, Nature Medicine.

[24]  S. Draibe,et al.  Incidence of and risk factors for hepatitis B virus and hepatitis C virus infection among haemodialysis and CAPD patients: evidence for environmental transmission. , 1995, Nephrology, Dialysis and Transplantation.

[25]  J. Garson,et al.  Hepatitis C virus infection in haemodialysis patients: a clinical and virological study. , 1994, Journal of Infection.

[26]  V. Carreño,et al.  Hepatitis GB virus C. , 1996, New England Journal of Medicine.