Hepatitis A, B, and C viruses are the most causative agents structural (core) and nonstructural proteins (NS3 and NS4) of infectious viral hepatitis worldwide. Hepatitis A virus of HGV produced in Escherichia coli. Seropositivity for HGV (HAV) is responsible for 32% of these infections, hepatitis B was evaluated and concordanced with HGV polymerase chain virus (HBV) for 44%, and hepatitis C virus (HCV) for 20%. 1 reaction (PCR) results in 709 subjects. These individuals were In 4%, the causative agent of infectious hepatitis is unknown. classified into a nonrisk or a risk group, on the basis of infec-A new agent was detected recently by molecular biological tion with human immunodeficiency virus (HIV) or hepatitis methods and was named hepatitis G virus (HGV).1 HGV is C virus (HCV) or frequent parenteral exposure, including about 9,400 bases long, a single-stranded, enveloped RNA hemophilia, intravenous drug addiction, receipt of blood virus, and like HCV it is a member of the Flaviviridae. HGV transfusion, or hemodialysis. The nonrisk group consisted of shares a nearly identical nucleotide sequence (ú98%) with 257 healthy blood donors with normal alanine transaminase another recently described virus: GB virus type C (GBV-C). 2,3(ALT) levels (ALT õ 30 U/L) and 154 patients with suspected Therefore, HGV and GBV-C seem to be isolates of the same non-A-E hepatitis (ALT ú 45 U/L). In the group of healthy virus. The HGV genome codes for structural proteins of the blood donors, 1.9% (5 of 257) had detectable HGV viremia viral core and envelope (core, E1, and E2) and for a number and 15.9% (41 of 257) showed antibody response to HGV. of nonstructural proteins (NS2-NS5) that are important durIn the collective of patients with suspected non-A-E hepatitis, ing viral replication. results from 1.9% of patients (3 of 154) were positive by HGV Until now, prevalence, clinical impact, and character of PCR, and 15.6% of patients (24 of 154) showed seropositivity antibody response regarding HGV infection were unclear. against the recombinant HGV proteins. In six groups of pa-Therefore, an immunoblot assay was established using retients (n Å 298) with different risk factors, the prevalence of combinant proteins from structural (core) and nonstructural both HGV viremia (V) and serological reactivity (SR) was regions (NS3 and NS4) of HGV produced in Escherichia coli. higher compared with that of the nonrisk group: V, 6.8%-To evaluate the prevalence of HGV infection, 709 individuals 35.2%; serological reactivity (SR), 25.4%-52.9%. The follow-were tested for both antibody response to HGV recombinant ing conclusions can be derived from our data. HGV infection proteins by the immunoblot assay and presence of HGV vireis widespread in the general population. The prevalence of mia by reverse transcriptase-polymerase chain reaction (RTantibodies against HGV or detectable HGV viremia is higher PCR). These 709 subjects differed in biochemical signs of in patients with risk factors for parenteral viral transmission hepatitis (alanine transamin...

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Of the various forms of chronic viral hepatitis, in Germany 60-70% are caused by the hepatitis C virus (HCV). The virus arrives inconspicuously, i.e. an acute infection only leads to an increase in transaminases in 40% of cases and to an increase in bilirubin in only 20%. However, approximately 90% of infections take a chronic course and in 20% this leads to cirrhosis after only 20 years. The infection rate of medical personnel is not significantly higher than in the general population. The transmission of HCV from patients to medical personnel, e.g. by needle stick injuries, is very rare and the risk of infection is less than 1%. Even less frequently transmission of HCV in the reverse direction from medical personnel to patients occurs. An active or passive prophylactic immunization is not possible and protective immunization is not yet foreseeable. Recently, progress has been made with chemotherapeutical treatment of HCV. The present state-of-the-art is pegylated interferon-a in combination with ribavirin. The success rate in HCV genotypes 2 and 3 is clearly higher with 70-80% than in genotypes 1 and 4 with approximately 40%. Both drugs have significant side-effects but better forms of medication are not yet available.