Hepatitis G virus biology, epidemiology, and clinical manifestations: Implications for blood safety

Authors
Citation
S. Kleinman, Hepatitis G virus biology, epidemiology, and clinical manifestations: Implications for blood safety, TR MED REV, 15(3), 2001, pp. 201-212
Citations number
97
Categorie Soggetti
Hematology
Journal title
TRANSFUSION MEDICINE REVIEWS
ISSN journal
08877963 → ACNP
Volume
15
Issue
3
Year of publication
2001
Pages
201 - 212
Database
ISI
SICI code
0887-7963(200107)15:3<201:HGVBEA>2.0.ZU;2-7
Abstract
Hepatitis G virus (HGV), also called GBV-C, is a single positive-standard R NA virus belonging to the Flaviviridae family. In 50% to 75% of infections, HGV is cleared with plasma RNA disappearing as anti-E2 becomes detectable; in other cases, HGV infection becomes chronic. The prevalence of HGV RNA i n blood donors ranges from 1% to 4%, and the rate of anti-E2, indicating re solved infection, ranges from 3% to 14%. HGV is transmitted by transfusion of blood components and has been transmitted by nonvirally inactivated fact or VIII concentrate. Despite extensive study, HGV has not been identified a s a causative agent of any type of liver disease or any other known clinica l condition. Molecular biology data show a lack of hepatotropism; prelimina ry data indicate that the site of HGV replication may be in mononuclear cel ls in bone marrow or spleen but not in peripheral blood or lymph nodes. The combined clinical and laboratory data strongly support the contention that HGV is not a hepatotropic virus and that this virus was inappropriately na med hepatitis G. Because the data do not indicate any pathologic effects of HGV, it is not appropriate to screen the blood supply for HGV RNA. Copyrig ht (C) 2001 by W.B. Saunders Company.