|
|
||||||||
Institut für Virologie Justus Liebig-Universität, Giessen, Germany
Proflavine inhibits DNA-dependent RNA synthesis in a way similar to actinomycin (1). It binds to DNA (2) and RNA (3, 4) and interferes with virus multiplication (4, 5). A dose-effect relationship has revealed that its binding capacity to DNA goes in parallel with the inhibition of cellular RNA synthesis and with the inhibition of the formation of fowl plague virus; while its binding capacity to RNA parallels the inhibition of protein synthesis and the inhibition of the formation of Newcastle disease virus (4). Therefore it has been suggested that proflavine inhibits fowl plague virus multiplication by the same mechanism as actinomycin does. The inhibition of Newcastle disease virus formation, however, should be due to an interference with an RNA template or t-RNA (6), inhibiting protein synthesis.
This investigation was concerned with the action of proflavine on the RNA-dependent RNA synthesis. The multiplication of Newcastle disease virus, strain ITALIEN, in primary chick fibroblast cells was chosen as a model.
* WHO research fellow, on leave from the Ivanovsky Institute of Virology, Moscow, U.S.S.R.
Received 30 May 1967;
accepted 17 June 1967.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| INT J SYST EVOL MICROBIOL | MICROBIOLOGY | J GEN VIROL |
| J MED MICROBIOL | ALL SGM JOURNALS | |