The Organism: HGV was discovered in 1996 by sequence analysis of a viral genome cloned form a patient with chronic non-A through E hepatitis. HGV is a single stranded RNA virus of the Flaviviridae family. It is approximately 75% homologous to the Hepatitis C virus. Despite its name, several well-designed studies documented that HGV does not cause any form of liver disease. Furthermore, there is no evidence to substantiate that the virus either infects or replicates in hepatocytes. In the case described here, the viral RNA was detected in the glomerular and tubular cells of the kidney, as well as in the PBMCs, which suggests these cells as the viral reservoir.

Laboratory Diagnosis and Epidemiology: The HGV RNA can be detected in serum or tissue specimens by reverse transcriptase, followed by polymerase chain reaction (RT-PCR). A serum ELISA assay is also available. This assay detects host antibody to HGV envelope protein E2. The HGV RNA is detectable as early as 2-3 weeks after exposure; patients develop anti-E2 at about the time when viremia clears, although in some the antibody is never detectable. HGV transmission by blood products has been definitively confirmed. The prevalence in donors ranges from 1 to 4.2%. High rates of HGV (20 to 30%) were documented in chronically transfused patients; even higher rates (75 to 95%) were seen in injection drug users. Maternal-fetal transmission rates vary from 60 to 80% in at least 5 studies. Although the virus can be detected in many patients, no clear pathologic role has been discovered to date, and consequently no screening protocols for blood and plasma donors have been implemented. Even though the current case demonstrates an association of HGV with MPGN, large studies of renal (as well as liver and heart) transplant patients failed to show any adverse effects on graft survival. This in contrast to Hepatitis C virus, where infection is clearly correlated to development of cryoglobulinemia and MPGN. Curiously, two studies of HIV patients showed slower rate of progression of HIV infection in HGV co-infected patients, although it is possible that this is due to a confounding variable and not the biologic effect of HGV.

Pouteil-Noble, C. et al. Glomerular disease associated with hepatitis C infection in native kidneys. Nephrol Dial Transplant;15S:28-33, 2000.

Berthoux, P et al. Membranoproliferative glomerulonephritis with subendothelial deposits (type I) associated with Hepatitis G infection in a renal transplant recipient. Am J Nephrol; 19:513-518,1999.