Curing of virus persistent infection in HVJ (sendai virus) carrier hamster tumor cells by transplantation

Transplantability of hamster tumor cells in the syngeneic system was considerably reduced by HVJ (Sendai virus) persistent infection of the cells, but these HVJ carrier cells still showed tumorigenicity, especially at high transplantation doses. Therefore, the existence of HVJ antigens or infectious...

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Veröffentlicht in:Gann 1981-08, Vol.72 (4), p.498-503
Hauptverfasser: Ogura, H, Sato, H, Hatano, M
Format: Artikel
Sprache:eng
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Zusammenfassung:Transplantability of hamster tumor cells in the syngeneic system was considerably reduced by HVJ (Sendai virus) persistent infection of the cells, but these HVJ carrier cells still showed tumorigenicity, especially at high transplantation doses. Therefore, the existence of HVJ antigens or infectious HVJ in the tumors formed in vivo by transplanted HVJpi (temperature-sensitive HVJ) or HVJo (non-temperature-sensitive HVJ) carrier tumor cells was examined in relation to the reduced transplantability of the cells. In stamp preparations of tumors cells, no HVJ antigens were detected from 14 days after transplantation, though they were positive if observed within 7 days. Infections HVJ particles could also be recovered from tumor tissues which were cocultivated with LLCMK2 cells within 7 days after transplantation. However, tumor cells recultured in vitro after more than 3 weeks post transplantation did not show HVJ antigens, even after various attempts at HVJ induction such as culture at low temperature, serial passages in vitro, treatment with 5-iododeoxyuridine, etc. The cytopathic effects and fluorescent antibody staining of these cells became positive when they were superinfected with wild-type HVJ, indicating a new establishment of HVJ infection after the curing of the HVJ genome initially carried. In contrast, the original HVJ carrier tumor cells were demonstrated to be completely resistant to this superinfection (one of the characteristics of persistent infection). These results seem to show that HVJ persistence in its carrier tumor cells was ultimately cured by transplantation and may provide at least a partial explanation of why the xenogenization of tumor cell by HVJ persistent infection was relatively weak.
ISSN:0016-450X