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.
D000818:Animals; D000998:Antiviral Agents / Q000494:pharmacology*; D002287:Carcinoma, Krebs 2 / Q000378:metabolism* / Q000382:microbiology; D002478:Cells, Cultured; D004591:Electrophoresis, Polyacrylamide Gel; D004686:Encephalomyocarditis virus / Q000254:growth & development* / Q000378:metabolism; D051379:Mice; D009363:Neoplasm Proteins / Q000096:biosynthesis*; D010670:Phenylthiourea / Q000031:analogs & derivatives* / Q000494:pharmacology; D014764:Viral Proteins / Q000096:biosynthesis*
D000998:Antiviral Agents; D009363:Neoplasm Proteins; D014764:Viral Proteins; C041099:N-phenyl-N'-3-hydroxyphenylthiourea; D010670:Phenylthiourea