Primaquine diphosphate: inhibition of Newcastle disease virus replication.
The response of Newcastle disease virus replication to primaquine, an antimalarial drug, was examined in chicken embryo cells (CEC). Virus-induced hemadsorption was completely inhibited by 250 mug of primaquine per ml. At lower concentrations, hemadsorption inhibition was dose dependent. Primaquine retarded virus-induced redistribution of receptor sites on the host cell plasma membrane as shown by the failure of infected, drug-treated CEC to be agglutinated with concanavalin A. The production of infectious progeny virus was substantially inhibited by the addition of primaquine at various times postinfection. When the drug was added early in the virus replication cycle, viral ribonucleic acid (RNA) synthesis was inhibited; however, when the drug was added late in the cycle, stimulation of RNA synthesis was observed. Primaquine was also shown to retard the incorporation of [(14)C]amino acids into proteins of virus-infected CEC. We suggest that the major role of primaquine is inhibition of protein synthesis; this results in changes in: hemadsorption, redistribution of lectin receptors, release of progeny, and virus-induced RNA synthesis.
D000371:Agglutination; D000818:Animals; D002642:Chick Embryo; D003208:Concanavalin A / Q000494:pharmacology; D005326:Fetal Proteins / Q000096:biosynthesis; D006382:Hemadsorption; D015394:Molecular Structure; D009522:Newcastle disease virus / Q000502:physiology*; D011319:Primaquine / Q000494:pharmacology*; D012313:RNA / Q000096:biosynthesis; D014779:Virus Replication / Q000187:drug effects*
D005326:Fetal Proteins; D003208:Concanavalin A; D012313:RNA; D011319:Primaquine