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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 ceils 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 in- hibition. Puromycin (33 o/~g./ml.) continued to protect > 9o ~ of the infected cells 24 hr after infection, while < 4o ~ of cells treated with cycloheximide (3oo #g./ml.) or streptovitacin A (3oo/~g./ml.) were protected from virus cytopathic effects at 24 hr. Seventy-five per cent inhibition of virus re- production was achieved with 24#g./ml. puromycin, oq25 #g.)ml. cyclo- heximide and 0.062/~g./ml. of streptovitacin A. When either puromycin (33o #g./ml.) or cycloheximide (3oo #g./ml.) was removed from infected cultures after a treatment period of 4 hr, cell rounding began shortly there- after and was complete I hr later. However, after the removal of strepto- vitacin A (3oo #g./ml.) there was a ~ 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-MK 2 cells in- fected with vaccinia virus the yield was 3 ° ~ of control 24 hr after infection. Virus yields from L2 cells treated with streptovitacin A, however, were only I to 5 ~ of control yields. The aminonucleoside of puromycin (33o #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).

Studies on the Mechanism of Vaccinia Virus Cytopathic Effects: Effect of Inhibitors of RNA and Protein Synthesis on Early Virus-induced Cell Damage