Failure to obtain drug-resistant variants of influenza virus after treatment with inhibiting doses of 3-deazaadenosine and H7.
3-Deazaadenosine and H7 specifically inhibit influenza virus replication under conditions at which they have no effect on other tested RNA viruses. This effect can be significantly potentiated by concomitant application of both compounds. Even under the most stringent conditions we failed to obtain any drug resistant variants. A possible explanation for this failure is that these compounds presumably do not act on a viral component like amantadine which was used as a control, but they interfere with cellular enzymes (factors) absolutely essential for influenza virus replication but more or less dispensable for the survival of the cell.
Scholtissek
C
C
Institut für Virologie, Justus-Liebig-Universität Giessen, Federal Republic of Germany.
Müller
K
K
D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D000818:Animals; D002478:Cells, Cultured; D002642:Chick Embryo; D004338:Drug Combinations; D004352:Drug Resistance, Microbial; D009980:Influenza A virus / Q000187:drug effects*; D007546:Isoquinolines / Q000494:pharmacology*; D010879:Piperazines / Q000494:pharmacology*; D014372:Tubercidin / Q000494:pharmacology*; D014779:Virus Replication / Q000187:drug effects
D004338:Drug Combinations; D007546:Isoquinolines; D010879:Piperazines; C018258:3-deazaadenosine; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D014372:Tubercidin