Vaccinia virus replication requires active participation of the host cell transcriptional apparatus.

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Abstract
The ability of vaccinia virus to replicate in BSC-40 monkey cells whose nuclei were functionally inactivated was examined. Exposure of cell monolayers to UV radiation at doses that did not alter the cells'' capacity to support a subsequent infection by a cytoplasmic virus (vesicular stomatitis virus) caused a reduction to less than 10% in the observed yield of infectious progeny from vaccinia virus and herpes simplex virus (type 1) infections. Similarly, replication of vaccinia virus was reduced to 5% by treatment of BCS-40 cells with .alpha.-amanitine (10 .mu.g/ml), a potent inhibitor of nuclear mRNA synthesis. In both situations, UV irradiation and .alpha.-amanitine treatment, early and late vaccinia viral genes were expressed at high levels, but the newly synthesized virion components were not assembled into mature infectious particles. Taken together, these data suggest that the active involvement of the host cell nuclear transcriptive system is obligatory in the vaccinia virus replicative cycle.