| Journal of General Virology |
| First posted online 19 July 2000 | ARTICLE ABSTRACT |
| Rec 23 February 2000; Acc 7 July 2000 | DOI: 10.1099/vir.0.16995-0 |
[Retraction published in JGV 82, part 11, 2837]
Atsushi Handa and Kevin E. Brown
Hematology Branch, National Heart, Lung and
Blood Institute, Bldg 10/Rm 7C218, National Institutes of Health, 9000
Rockville Pike, Bethesda, MD 20892-1652, USA
A novel flavivirus, GB virus C (GBV-C)/hepatitis G virus (HGV), has been detected in chronic liver disease patients. It is known that the viral RNA can be detected in ~5 % of American blood donors. However, the implications for liver disease and the sites of virus replication remain unknown. Possible sites of virus replication were studied by using cell lines and/or primary cells derived from human lymphoid cells, myeloid cells, hepatocytes and endothelial cells. RNA was detected by virus strand-specific RTPCR and GBV-C/HGV antigen was detected with a rabbit polyclonal anti-E2 (envelope 2) antibody by Western blot analysis. Negative-strand RNA, representative of replicating virus, was detected in lymphoid and megakaryocytoid cell lines and primary vascular endothelial cells. In addition, an increase in virus titre over time was demonstrated and viral antigen was detected, and virus could be passaged to infect fresh cells. However, viral RNA or antigen could not be detected in any of the hepatocyte lines tested. These results indicate that the replication site of GBV-C/HGV is not primarily in hepatocytes and that detection of replicating virus in hepatic tissue may reflect virus replication in haematopoietic cells and/or vascular endothelial cells present in the liver.
This article is now available in the October 2000 print issue of JGV (vol. 81, 2461-2469). The complete issue of the journal may be seen in electronic form on JGV Online.