Abstract
Two mutants of vaccinia virus, one resistant and the other dependent on isatin-β-thiosemicarbazone (IBT), were isolated and characterized. Complementation took place when these mutants and the wild-type strain were co-cultivated. Genetic recombination was carried out between the IBT-resistant and a temperature-sensitive mutant of vaccinia virus. IBT affects vaccinia virus growth at a step during the maturation of the virus particles; cleavage of high molecular weight precursors, giving rise to viral polypeptides, is inhibited under these conditions. Biochemical and electron microscopy observations suggested that IBT blocks the maturation of the wild-type strain of vaccinia virus later than rifampin. The growth of the IBT-dependent mutant is interrupted in the absence of IBT at a similar stage of maturation. All seventeen compounds studied until now, that are related in their structure to IBT, which inhibited the growth of vaccinia virus and to which the IBT-resistant mutant showed resistance in its growth, were able to support the growth of the IBT-dependent mutant.
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