Abstract
Actinomycin D inhibited the yield of influenza virus hemagglutinin from MDCK cells infected at high multiplicity, but had little effect on the yield of parainfluenza virus hemagglutinin. In similar hemagglutinin yield experiments, ribavirin was only slightly more active (threefold) against influenza virus than against parainfluenza virus replication. In plaque inhibition experiments, ribavirin depressed influenza virus plaque formation by 50% at a concentration of approximately 3 micrograms/ml, whereas the corresponding figure for parainfluenza viruses was threefold higher. The concentration of ribavirin demonstrating anti-influenza activity was indistinguishable for that inhibiting host cell growth. It is concluded that, unlike actinomycin D, ribavirin is unlikely to have a major effect on the provision of host cell 5-germinal methylated cap structures and the subsequent priming of influenza messenger ribonucleic acid synthesis.