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Summary Infectivity titration, sedimentation analysis in sucrose gradients and electron microscopy have been used to study virus maturation following the reversal of the inhibition of vaccinia virus growth by rifampicin. Electron-dense inclusions containing tubular structures develop in the cytoplasm of infected BHK 21/C 13 cells maintained in rifampicin, but the formation of immature and mature virus particles is prevented. The removal of rifampicin is followed by a rise of the virus infectivity. Spicule-covered membranes appear at the periphery of the inclusions and both immature and mature virus particles are seen. A proportion of the DNA synthesized in the presence of rifampicin is incorporated into particles and becomes resistant to deoxyribonuclease I. If protein synthesis is inhibited, spicule-covered membranes and immature particles appear but no mature particles are seen; the virus infectivity does not increase and the DNA remains susceptible to deoxyribonuclease I. It is suggested that rifampicin binds reversibly to a virus-specified protein, thereby preventing the formation of immature virus particles. Possible effects of rifampicin on the subsequent stages of virus maturation are discussed.

Events in Vaccinia Virus-infected Cells Following the Reversal of the Antiviral Action of Rifampicin