We have described a novel gene transfer system, in which subcutaneously into mice every 4 weeks. These mice were replication-incompetent, T antigen-deleted simian virus-40 bled every 2 weeks and their sera assayed for antibody (SV40) is used as the transduction vehicle. We report here activity against HBsAg and SV40. Production of anti-HBs successful immunization using such an SV40-derived viral was measured by ELISA and confirmed by Western blot vector. Hepatitis B surface antigen (HBsAg) cDNA was analysis, both of which demonstrated significant levels of cloned downstream of two tandem SV40 early promoters anti-HBs after the second injection. We also tested proto yield a T antigen-deficient SV40 derivative, SV(HBS).duction of anti-SV40 antibodies by the ability of sera to Cultured TC7 cells were exposed to SV(HBS), and neutralize SV(HBS) infectivity. We found no evidence of expression of HBsAg was detected 24 h later by Northern neutralization of SV(HBS) infectivity even after eight inocublot and RT-PCR analysis. Immunochemistry and Western lations. Thus, replication-incompetent SV40 is itself not a blot analysis were also performed 24 h after infection to strong antigen. Our data suggest that SV40-based transdetect expression of HBsAg. Once it was ascertained that duction systems may be a useful vehicle for immunization we could express HBsAg in this way, we used SV(HBS) to and for other gene transfer applications when a need for elicit anti-HBs. SV(HBS) was injected intraperitoneally or multiple inoculations is anticipated.

Studies were carried out to test the hypothesis that exposure to aflatoxin B1 (AFB1) is common among individuals with hepatocellular carcinoma (HCC) who are also chronically infected with hepatitis B virus (HBV). Experiments were also carried out to determine whether there is a close association between the presence of AFB1-DNA adducts and the expression of one or more HBV antigens in the tumor or non-tumor regions of the liver. Twenty-seven paired tumor and non-tumor liver tissues of HCC patients from Taiwan were analyzed. Monoclonal antibody 6A10, generated against the imidazole ring-opened persistent form of the major N-7 guanine adduct of AFB1, was used for adduct detection by both indirect immunofluorescence and competitive enzyme-linked immunosorbent assay. An avidin-biotin complex staining method was used for the detection of HBsAg and HBxAg in liver sections. A total of 8 (30%) HCC samples and 7 (26%) adjacent non-tumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent non-tumorous liver samples were positive while 9 (33%) HCC samples and 11 (41%) adjacent non-tumor liver samples were HBxAg-positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These results suggest that both AFB1 exposure and carrier status of HBsAg/HBxAg may be involved in the induction of HCC in Taiwan.

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