Key result
Some rifamycin-related compounds strongly inhibited vaccinia virus DNA-dependent RNA polymerase in vitro at concentrations of 150 mug/ml or less, though this effect differed from the in vivo effect.
Rifamycins and related antibiotics can inhibit vaccinia virus RNA polymerase in vitro, but this effect differs from their in vivo mechanism of action.
Rifamycin compounds' in vitro vaccinia polymerase inhibition does not support clinical antiviral use; leaves open in vivo mechanism and efficacy questions.
A number of compounds related to rifampin which act as expected in the Escherichia coli system have been tested for their ability to inhibit the vaccinia particle deoxyribonucleic acid-dependent ribonucleic acid (RNA) polymerase in vitro. Some compounds are inactive even at concentrations of 500 mug/ml, others are able to produce partial inhibition, and others strongly inhibit the enzyme activity at 150 mug/ml or less. The inhibition, where present, operates immediately but appears to be at least partially reversible. At least one compound which is without effect against bacterial RNA polymerase is a potent inhibitor of the viral RNA polymerase. As the enzyme activity of rifampin-resistant mutants of vaccinia virus is inhibited to the same extent as that of the wild type, the observed in vitro effect on vaccinia virus RNA polymerase is not identical with the in vivo effect specifically directed against a vaccinia-specified protein.
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Szilágyi et al. (1971) studied Vaccinia virus. Rifamycins and related antibiotics was evaluated on Inhibition of vaccinia particle deoxyribonucleic acid-dependent ribonucleic acid (RNA) polymerase in vitro. Some rifamycin-related compounds strongly inhibited vaccinia virus DNA-dependent RNA polymerase in vitro at concentrations of 150 mug/ml or less, though this effect differed from the in vivo effect.
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