Influenza cellular mechanisms

MECHANISMS OE ACTION AND RESISTANCE Ribavirin alters cellular nucleotide pools and inhibits viral mRNA synthesis. Intracellular phosphorylation to the mono-, di-, and triphosphate derivatives is mediated by host cell enzymes. In both uninfected and RSV-infected cells, the predominant derivative is the triphosphate, which has an intracellular of <2 hours. Ribavirin monophosphate competitively inhibits cellular inosine-5 -phosphate dehydrogenase and interferes with the synthesis of GTP and thus nucleic acid synthesis. Ribavirin triphosphate also competitively inhibits the GTP-dependent 5 capping of viral messenger RNA and specifically influenza virus transcriptase activity. Ribavirin has multiple sites of action, and some of these e.g., inhibition of GTP synthesis) may potentiate others e.g., inhibition of GTP-dependent enzymes). Ribavirin also may enhance viral mutagenesis such that some viruses may be inhibited in effective replication, so-caUed lethal mutagenesis. 

Viruses are minute non-cellular organisms which can only reproduce within a host cell. They are very much smaller than bacteria and cannot be controlled by antibiotics. They appear in various shapes and are continually developing new strains. They are usually only defeated by the defence and healing mechanisms of the body. Drugs can be used to relieve the symptoms of a viral attack but cannot cure it. The common cold is a viral infection as are hepatitis, AIDS (HIV) and influenza. 

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