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Although the hepatitis G virus is unlikely to be a primary hepatotropic virus, its replication sites remain unclear. Using highly strand-specific Tth-based reverse transcriptase PCR we searched for the presence of the viral RNA negative strand in various autopsy tissues in two patients who died of end-stage liver disease. In addition, amplified viral sequences were compared in the 5' untranslated and the putative capsid regions by the single-strand conformation polymorphism (SSCP). Negative strand HGV RNA was detected in bone marrow and spleen from both patients and in lymph node tissue from one. All amplified sequences from a given patient were identical when compared by SSCP and direct sequencing. This lack of difference in the composition of quasispecies recovered from various tissues suggests the presence of a single, common viral compartment in the infected host.

Hepatitis B virus (HBV) is the major etiological agent of hepatocellular carcinoma (HCC). Whether any particular viral variants are associated with HCC is unknown. We studied 53 Gambian patients with HCC and 33 HBsAg positive controls. A functional part of HBV core promoter and whole precore region were sequenced directly and/or after cloning. HBV DNA was amplified from sera from 27 HCC patients and in all controls. Fourteen (52%) patients and 12 (36%) controls (NS) were found to harbor an HBV strain with G to A transition mutation at position 1896 leading to HBeAg negative phenotype. Nine (33%) HCC patients and 2 (6%) controls (p < 0.01) harbored a mixture of wild type and HBV strains with deletions/insertions; strong consensus sequences for topoisomerase I breakage were located in the vicinity of these changes. In Africa, HCC is associated with HBV strains that have deletions/insertions in the HBV core promoter region.