Abstract
The sites and mechanisms of action of both the activity and the resistance to antiviral drugs have been characterized more precisely than have those for any other class of drugs (Richman, 1994a). The next step is the rational translation of our understanding of the pathogenesis of viral diseases and the responses of virus replication to intervention with antiviral drugs in the design of combination regimens for the durable, effective control of viral disease. Drug treatment selects for the emergence of resistant mutants. For single stranded RNA viruses, whose genomic replication lacks a proofreading mechanism, the mutation frequencies are approximately 10 -‘. Thus, a single lo-kilobase genome, like that of human immunodeficiency virus (HIV), would be expected to contain on average one mutation in each progeny viral genome. Many virus infections are characterized by high levels of virus replication with high rates of virus turnover. This is especially true of the chronic infection with HIV, hepatitis B virus
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