Clinical implications of hepatitis G virus (HGV) infection in patients of acute viral hepatitis & fulminant hepatic failure

Background & Objectives: Viral hepatitis is a major public health problem especially in developing countries such as India. Hepatitis viruses A, B, C, D and E are all well characterized and molecularly defined agents with unequivocal association with human liver disease but there is evidence of hepatitis in humans caused by certain transmissible agents which cannot be classified with the above hepatotoric viruses. The role of recently discovered hepatitis G virus (HGV/GBV-C) as an independent heaptitis agent is controversial. Recently, we have shown a relatively high frequency of HGV infection in fulminant hepatic failure but the virus was often detected in co-infection with hepatitis B or E virus. The present study has therefore been carried out to evaluate the clinical significance of HGV infection in acute viral hepatitis (AVH) and fulminant hepatic failure (FHF) through follow up of HGV positive patients till their clinical and biochemical recovery. Methods: The study included 50 patients comprising 35 of AVH and 15 of FHF. These patients were evaluated on the basis of history, physical examination, liver function profile and serological markers for hepatitis A, B, C and E. Those patients serologically negative for HBV and HCV infection were further screened for HBV DNA and HCV RNA by PCR. All the samples were screened for presence of HGV-RNA by RT-PCR using inner and outer primers sequences selected from NS3 helicase region of the HGV genome. FHF patients who died were subjected to postmortem liver biopsy and these biopsy specimens were also screened for HGV-RNA. Repeat detection of HGV-RNA was done after clinical and biochemical recovery of the patients. Results: Of 35 AVH patients, HGV infection was detected in 5 patients (14.3%) while 4 of 15 patients (26.6%) in the FHF group were positive for HGV-RNA. Five HGV positive AVH patients were followed till clinical and biochemical recovery and all of them tested positive for HGV-RNA at follow up (6 weeks to 6 months). Out of 4 HGV positive FHF patients, only one survived and his repeat sample after clinical and biochemical recovery tested positive for HGV-RNA. INTERPRETATION & Conclusions: The results suggest that HGV infection does occur in patients of AVH and FHF and HGV viraemia persists for a long time even after clinical and biochemical recovery. These observations point towards a possible non-pathogenic role of hepatitis G virus infection