The parvovirus, H-1, undergoes an abortive cycle of growth in secondary human embryonic lung (HEL) cell cultures, but replicates in several stable cell lines of human origin (Toolan & Ledinko, 1965; Toolan, 1968). In HEL cells, H-1 infection causes the formation of capsid proteins, without the production of infective virus (Ledinko, Hopkins & Toolan, 1969). Mixed infection with human adenovirus type 12 allows H-1 virus to complete its development (Ledinko & Toolan, 1968; Ledinko, Hopkins & Toolan, 1969). At present, the events of the adenovirus growth cycle required for H-1 virus are not known. The restriction in HEL cells of H-1 virus, which contains single-stranded DNA (Usategui-Gomez 1969), may involve an inhibition of viral DNA synthesis. It is possible that some enzyme concerned with DNA synthesis, and induced by adenovirus, can function in the synthesis of active H-1 virus.


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