Hepatitis G virus infection in acute fulminant hepatitis: prevalence of HGV infection and sequence analysis of a specific viral strain

• Published in: Journal of viral hepatitis Vol. 5; no. 5; pp. 301 - 306
• Main Authors: Sheng, L., Soumillion, A., Beckers, N., Wu, C.-G., Verslype, C., Nevens, F., Pirenne, J., Aerts, R., Kosala, H., Fevery, J., Yap, S. H.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.09.1998
• Subjects: Adolescent; Adult; Aged; Base Sequence; Blood Donors; Female; Flaviviridae - genetics; Flaviviridae - isolation & purification; fulminant hepatitis; Hepatic Encephalopathy - blood; Hepatic Encephalopathy - virology; Hepatitis G virus; Hepatitis, Viral, Human - blood; Hepatitis, Viral, Human - epidemiology; Hepatitis, Viral, Human - virology; Humans; Male; Middle Aged; Molecular Sequence Data; Mutation; Polymerase Chain Reaction; Prevalence; RNA, Viral - blood; Sequence Alignment
• ISSN: 1352-0504; 1365-2893
• DOI: 10.1046/j.1365-2893.1998.00123.x

Hepatitis G virus (HGV) is a recently discovered RNA virus, which belongs to the Flaviviridae family. Although HGV infection is usually not associated with elevated serum transaminases, some recent studies have reported that HGV infection is found in a significant number of patients with fulminant hepatitis and may play a role in its etiopathogenesis. In this study the prevalence of HGV infection was determined in 500 healthy blood donors and in 24 patients admitted to hospital because of acute liver failure caused by fulminant hepatitis. The presence of HGV RNA was tested in sera, obtained at admission and before any transfusion was given, by a sensitive seminested reverse transcriptase–polymerase chain reaction (RT–PCR) assay specific for detection of the non‐structural (NS)5 region. Nine of the 500 blood donors (1.8%) and two of the 24 patients (8.3%) were found to be HGV RNA positive. One patient was co‐infected with HCV and was known to be an intravenous (i.v.) drug user. After intensive supporting treatment, this patient recovered completely. The second patient had no serological markers of known viral hepatitis infection, including hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), cytomegalovirus (CMV), Epstein–Barr virus (EBV) and herpes simplex virus (HSV). This patient was successfully transplanted. From both patients, from HGV RNA‐positive healthy blood donors and from other patients coinfected with HCV, a part of the HGV NS3 region (nucleotides 4191–4345, EMBL entry U45966) was cloned and sequenced. Sequence comparison revealed that the NS3 region of HGV in patients with fulminant hepatitis contained three nucleotide substitutions as part of the six substitutions described in previous work. These nucleotide substitutions were not found in the tested blood donors or in patients with HCV co‐infection. Our findings therefore support the concept of the association of fulminant hepatitis with infection of a specific HGV strain.