Abstract
PERMISSIVE cell systems for the replication of the Epstein–Barr virus (EBV) and some of the related EBV-like agents (for example, Herpesvirus papio and herpesvirus pan) have not yet been established1. EBV is regularly demonstrated in a small number of cells from lymphoblastoid lines of B-cell origin which have been derived from certain lymphoma patients, most frequently from Burkitt's lymphoma or patients with infectious mononucleosis, but also from healthy EBV-reactive individuals. EBV DNA usually persists in cells of these lines in multiple copies2–4, but spontaneous induction of viral antigens and particle synthesis occurs in a majority of the lines at a low rate. To some extent, the percentage of induced cells seems to be cell line-specific1, and two lines which are rather high producers of EBV are the P3HR-I line of BL origin5 and the marmoset B95-8 line isolated from lymphocytes transformed with EBV of infectious mononucleosis origin6. At any time during cultivation, 2–10% of the cells reveal viral capsid antigen synthesis as determined by indirect immunofluorescence7. All attempts to increase the virus yield in these lines by temperature shifts or chemical or physical inducers (IUdR, mitomycin C, X rays) have usually resulted in only barely significant enhancement of viral replication8–10. We now report on a very efficient induction of EBV and other oncogenic herpesviruses by the well established cocarcinogen and tumour promoter 12-O-tetra-decanoylphorbol-13-acetate (TPA)11. In addition some TPA-treated cells show cytopathogenic changes, including polyploidisation. These observations may enable a more complete investigation of the virus-cell-gene balance hypothesis12.
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HAUSEN, H., O'NEILL, F., FREESE, U. et al. Persisting oncogenic herpesvirus induced by the tumour promoter TPA. Nature 272, 373–375 (1978). https://doi.org/10.1038/272373a0
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DOI: https://doi.org/10.1038/272373a0
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