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Antiviral drugs have been developed that work by the following mechanisms: inhibition of the synthesis of viral DNA, RNA and proteins (for example, nucleoside analogues, reverse transcriptase inhibitors, protease inhibitors); reduction in release of viral genetic material once inside the host cell (for example, amantadine); interference with penetration of virus through the cell membrane (for example, neuraminidase inhibitors); interference with attachment of the virus to the host cell membrane (for example, vaccines, immunoglobulins and interferons). Resistance can occur through a number of consequences of viral mutation. There may be reduced phosphorylation of the drug, alteration of viral enzyme targets, or alteration of target channel protein. These synthetic compounds resemble the natural nucleotides of viral DNA or RNA. They are phosphorylated in infected cells and then compete with the normal nucleotides for incorporation into viral DNA or RNA.

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With prolonged use of anti-inflammatory corticosteroids, the adrenal glands atrophy and lose their ability to synthesize their natural corticosteroids. If the corticosteroid drugs are stopped and the adrenal glands are no longer able to produce sufficient natural corticosteroids, the body will be unable to withstand every day stresses, a situation that can be life threatening. Anti-inflammatory corticosteroids depress the immune system. Response to infection can be severely impaired as a result of inhibition of the activity of leukocytes and reduction in their numbers.

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Authored by Dr. Andrew L. Schechterman, PHD


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