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
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.