**2.11. Ribavirin (1-ß-D-ribofuranosyl-1,2,4-triazole-3-carboxamide)**

This triazole nucleoside was described initially by Sidwell et al. [35]. Numerous studies were carried out on the mode of action of this compound manifesting activity toward large spectrum of viruses (predominantly RNA containing) belonging to different taxonomic groups. However, there are no data about the mechanism of anti-AdV effect of ribavirin. Several different mechanisms were formulated about the antiviral effects of this compound: (1) decreased levels of intracellular guanosine triphosphate pools based on inhibition of cellular inosine-5-monophosphate dehydrogenase; (2) inhibition of viral polymerases; (3) inhibition of RNA capping activity of viral transcripts; (4) lethal mutagenesis of the viral RNA genomes, also termed "error catastrophe," based on the induction of increased viral mutation rate over the critical error rate (especially expressed on enterovirus replication) via incorporation of the compound into newly synthesized genomes; (5) immunomodulatory role particularly on adaptive immune responses—the compound is inducer of the helper-T-cell type 1 cytokine response, but also a suppressor of the type 2 cytokine phenotype. Data about anti-AdV effect in cell culture experiments are very controversial. It was established that its activity is limited to AdVs of group C and strongly cell culture-dependent [36]. However, the plasma concentrations reached by ribavirin are 10 times below the required IC50 value [36, 37].
