Effect of N-phenyl-N'-3-hydroxyphenylthiourea (PTU-23) on the protein synthesis in Krebs-II cells infected with encephalomyocarditis virus.

PTU-23, a selective inhibitor of the reproduction of encephalomyocarditis (EMC) virus in Krebs-II ascites carcinoma cells, counteracts the virus-induced shut-off of the host-cell protein synthesis reducing it from 32% to 19%. The compound does not inhibit the synthesis of virus-specific proteins; the electrophoretic profile in SDS-PAAG shows an increase in the peaks of some viral polypeptides, mainly A, E and epsilon. It is suggested that this effect is connected to the partial inhibition by PTU-23 of the synthesis of the viral 37S RNA, without affecting its translation activity and also to the inhibition of the synthesis of 20S (RF) RNA--an inhibitor of the virus-specific protein synthesis. PTU-23 does not affect the processing of the high-molecular-weight viral precursor polypeptide preA, which is carried out by the virus-specific protease protein p22, as shown in studies with a cell-free system.