Effects of actinomycin D on the cytopathology induced by poliovirus in HEp-2 cells.
One possible mechanism of virus-induced cell damage is that the redistributed (released) lysosomal enzymes produce the cytopathic effect during cytolytic types of infections such as poliovirus in HEp-2 cells. To determine if the lysosomal enzyme redistribution and cell damage are host-cell directed, we studied sensitivity of these events to the action of actinomycin D. By the use of actinomycin D at concentrations producing the least toxicity but maximal effectiveness in shuting down cell RNA synthesis, it was shown that the cytopathic effect and enzyme redistribution were not inhibited and, therefore, not directly controlled and induced by the cell genome in response to the virus infection. Evaluation of cytopathic effect by a phase contrast microscopy method detected changes earlier than the erythrocin B uptake method.
D002294:Carcinoma, Squamous Cell; D002458:Cell Fractionation; D002460:Cell Line; D003588:Cytopathogenic Effect, Viral / Q000187:drug effects*; D003609:Dactinomycin / Q000494:pharmacology*; D004917:Erythromycin / Q000378:metabolism; D005696:Galactosidases / Q000378:metabolism; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D007822:Laryngeal Neoplasms; D008247:Lysosomes / Q000201:enzymology; D008858:Microscopy, Phase-Contrast; D017955:Poliovirus / Q000254:growth & development*; D012334:RNA, Neoplasm / Q000096:biosynthesis; D014316:Tritium; D014529:Uridine / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects
D012334:RNA, Neoplasm; D014316:Tritium; D003609:Dactinomycin; D004917:Erythromycin; D005696:Galactosidases; D005966:Glucuronidase; D014529:Uridine