1887

Abstract

Summary

The ihd strain of vaccinia virus caused the rounding of all LLC-MK2 cells in a culture within 2 to 4 hr after infection. One g./ml. of either cycloheximide or streptovitacin A protected 75 % of the infected cells from early cytopathic effects occurring 4 hr after infection and treatment. As much as 83 g./ml. of puromycin was required to achieve the same degree of inhibition. Puromycin (330 g./ml.) continued to protect > 90 % of the infected cells 24 hr after infection, while < 40 % of cells treated with cycloheximide (300 g./ml.) or streptovitacin A (300 g./ml.) were protected from virus cytopathic effects at 24 hr. Seventy-five per cent inhibition of virus reproduction was achieved with 24g./ml. puromycin, 0·125 g./ml. cycloheximide and 0·062g./ml. of streptovitacin A. When either puromycin (330 g./ml.) or cycloheximide (300 g./ml.) was removed from infected cultures after a treatment period of 4 hr, cell rounding began shortly thereafter and was complete 1 hr later. However, after the removal of streptovitacin A (300 g./ml.) there was a 1 hr delay before virus cytopathic effects appeared. The cytopathic effects reached maximum 3 hr after the removal of the compound. When streptovitacin A was removed from LLC-MK2 cells infected with vaccinia virus the yield was 30 % of control 24 hr after infection. Virus yields from L2 cells treated with streptovitacin A, however, were only 1 to 5 % of control yields. The aminonucleoside of puromycin (330 g./ml.) markedly inhibited virus replication, but did not significantly alter the development of virus cytopathic effects.

These findings are taken as further evidence that the early cytopathological effects induced by vaccinia virus result from the synthesis of virus-induced protein(s).

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1970-02-01
2024-03-29
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