Abstract
Summary
The effect of 2 purine analogs, 2,6-diaminopurine (DP) and 8-azaguanine (AZA) on the multiplication of encephalomyocarditis (EMC) and vaccinia viruses in analog-sensitive and -resistant strain L cells has been investigated. It was shown that DP and AZA inhibit the multiplication of both viruses in analog-sensitive cells. DP does not inhibit the replication of EMC and vaccinia viruses in DP-resistant cells. The mechanism of cellular resistance to this analog might prevent the inhibitory action of DP on viral replication. On the other hand, AZA inhibits virus growth in AZA-resistant cells as well as in analog-sensitive cells. The mechanism of cell resistance is not effective in protecting viral replication from the inhibitory effect of the analog. It is suggested that the cell resistance to AZA may be at a step following ribophosphorylation and that virus-specific RNA synthesis might be affected by the antimetabolite, whereas cellular RNA synthesis is not significantly inhibited by the analog nucleotide.
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