The basis for accumulation of capsid antigen in the cytoplasm of cells infected with a newly recognized variant of polyoma has been investigated. The virus progeny and the infectious cycle were compared with that of a normal large plaque strain (lp-s). No significant differences to account for the variation were observed. Expression of this phenotypic character was modified by reduced temperature of incubation combined with serum or arginine deprivation or independently by treatment of infected cells at specific times post-infection with 5-fluorodeoxyuridine actinomycin D or Actidione (cycloheximide).

These results are compatible with the hypothesis that accumulation of capsid antigen in the cytoplasm results from its synthesis at a rate greater than its diffusion into the nucleus. The molecular basis of the defect is discussed.


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