Distribution of hepatitis G viremia and antibody response to recombinant proteins with special regard to risk factors in 709 patients

✍ Scribed by H Feucht; B Zollner; S Polywka; B Knodler; M Schroter; H Nolte; R Laufs

• Book ID: 102244877
• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 215 KB
• Volume: 26
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.510260234

✦ Synopsis

mia and clinical or biochemical signs of hepatitis in A new virus named hepatitis G virus (HGV) has been deindividuals without risk factors for acquiring parenterally tected recently. Until now, no assays for the detection of transmitted agents. (HEPATOLOGY 1997;26:491-494.) antibodies against different HGV proteins have been commercially available. Therefore, a strip immunoblot assay has been established to investigate seroreactivity against recombinant

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 dur-In 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 followwere 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 transaminase [ALT] levels) and in the presthan in those without risk factors. The majority of HGV infecence of risk factors for acquiring parenterally transmitted tions (70.2%) is self-limiting and not persistent in our collecagents. tive of patients. We found no correlation between HGV vire-

PATIENTS AND METHODS

Patients. Sera drawn from 709 individuals were examined for the Abbreviations: HGV, hepatitis G virus; GBV-C, GB virus type C; ALT, alanine presence of HGV-RNA and serological reactivity against recombitransaminase; PCR, polymerase chain reaction; HAV, hepatitis A virus; HBV, hepatitis nant HGV proteins. The patients were 17 to 76 years old; the median B virus; HCV, hepatitis C virus; RNA, ribonucleic acid; RT, reverse transcriptase; HIV, human immunodeficiency virus; IVDA, intravenous drug addiction; cDNA, comple-age was 41.6 years; 418 (59.0%) were male, and 291 (41.0%) were mentary deoxyribonucleic acid; SIBA, strip immunoblot assay.

female.