EPIDEMIOLOGIC AND CLINICAL ASPECTS OF HEPATITIS-G VIRUS-INFECTION IN BLOOD-DONORS AND IMMUNOCOMPROMISED RECIPIENTS OF HGV-CONTAMINATED BLOOD

Citation
Hg. Heuft et al., EPIDEMIOLOGIC AND CLINICAL ASPECTS OF HEPATITIS-G VIRUS-INFECTION IN BLOOD-DONORS AND IMMUNOCOMPROMISED RECIPIENTS OF HGV-CONTAMINATED BLOOD, Vox sanguinis, 74(3), 1998, pp. 161-167
Citations number
24
Categorie Soggetti
Hematology
Journal title
ISSN journal
00429007
Volume
74
Issue
3
Year of publication
1998
Pages
161 - 167
Database
ISI
SICI code
0042-9007(1998)74:3<161:EACAOH>2.0.ZU;2-A
Abstract
Background and objectives: The infectiousness and clinical relevance o f the newly discovered blood-borne Flaviviridae-like agent, termed hep atitis G virus (HGV), are not well understood. Materials and methods: Twenty-three transfusion recipients of two HGV-affected long-term bloo d donors were studied for HGV genome and antibodies to the putative en velope 2 glycoprotein (anti-E2) of HGV. Nine recipients had nonhematol ogical disorders and 14 suffered from severe hematological diseases an d 7 of them received allogeneic bone marrow or blood stem cell transpl antation. The molecular epidemiology of the observed HGV infection was studied by direct sequencing of parts of the 5'-noncoding region, NS3 , and NS5 region of HGV in the 2 long-term donors and in their 6 recip ients who became HGV RNA positive. Additionally, 549 individuals-homol ogous (n = 254) and autologous blood donors (n = 202), and medical sta ff (n = 89)-were investigated for the presence of HGV RNA. Results: HG V RNA in serum was found in 15 of the 23 (65%) transfusion recipients with known exposure of HGV-contaminated blood. Seven of the remaining 8 recipients showed only an anti-E2 response, indicating previous HGV infection with spontaneous clearance of the virus. In one recipient ne ither HGV RNA nor anti-E2 could be detected. Molecular evidence for HG V transmission by the 2 donors was found in 3 of the 6 recipients stud ied. The alanine aminotransferase levels were not significantly differ ent in the HGV RNA positive and negative recipients, and none of the 2 3 recipients developed posttransfusion hepatitis. Persistent HGV infec tion was observed especially in recipients with severe hematological d isorders or in those in whom intensive immunosuppressive treatment was necessary. Of the 549 individuals studied, 10 (1.8%) were healthy car riers of HGV RNA. Conclusion: The persistence of transfusion-acquired HGV infection is not associated with acute or chronic hepatitis, but m ay be influenced by the recipient's underlying disease.