E. Various Inhibitors
V. RNA-DEPENDENT DNA SYNTHESIS
The presence of RNA-dependent D N A polymerase in R N A tumor viruses was first reported by Temin and Mizutani (232) and Baltimore
(283). The replication of the nucleic acid of R N A tumor virus was known to be different from that of other R N A viruses from the results of early experiments with various inhibitors, e.g., the sensitivity of virus production, infectivity, and growth of Rous sarcoma virus to actinomycin D , which is not inhibitory to RNA-dependent R N A polymerase.
iV-Demethylrifampicin, an analog of rifampicin, has been found by M. Green (see ref. 234) to inhibit the RNA-dependent D N A polymerase of oncogenic R N A virions. Partially purified RNA-dependent D N A poly
merase from human acute lymphoblastic leukemic cells has also been found to be markedly inhibited by Λ^-demethylrifampicin and inhibited much less by rifampicin itelf (234). Streptovaricin, on the basis of its analogous action to rifampicin, has been tested for its possible inhibitory activity against RNA-dependent D N A polymerase isolated from murine leukemia virus. Streptovaricin complex (a mixture of seven macrolides) proved to be an extremely potent inhibitor of the purified RNA-depen
dent D N A polymerase from the oncogenic virus (235).
The significance of the RNA-dependent D N A polymerase for carcino
genesis by R N A viruses is still not fully understood. However, if the presence of this enzyme is really unique to neoplastic cells, then its inhibition by agents such as N-demethylrifampicin or streptovaricin has obvious implications for chemotherapy. The search for more specific inhibitors of this enzyme should give good hope for successful chemother
apy of RNA-virus-induced cancer and, maybe, of other diseases such as neurological disorders caused by R N A viruses.
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