Garret writes:
> I would wonder if the targeted virus would mutate in response to the treatment and then what? Is that a reasonable question?

Viral evolution

Viruses replicate extremely rapidly and accumulate mutations and short deletions, particularly viruses with life cycles that involve RNA genomes. As discussed in further detail below, since RNAi relies upon nearly perfect sequence identity between an siRNA guide and the mRNA target, the accumulation of mutations can render a virus resistant to RNAi suppression, analogous to the evolution of viral resistance to HAART [antiretroviral therapy]. 

Furthermore, during viral replication, dsRNA encoding viral proteins or the full genome is often generated, potentially exposing the virus to host cell RNAi. As a result, it is not surprising that numerous viruses have evolved efficient suppressors of RNAi. Although this phenomenon is better characterized in plant infections than in animal viruses,1 the apparent presence of RNAi suppressors in human viruses indicates that they could impact antiviral RNAi strategies.

One drawback to targeting viral genes with RNAi is that viral mutation can lead to a loss of sensitivity to RNAi. This is an especially problematic possibility for the cases of RNA viruses, which accumulate point mutations up to 107-fold more rapidly than do their counterparts with DNA genomes.

Although most of these mutants achieved resistance through point mutation or deletion of the target sequence, one HIV mutant escaped RNAi suppression by accumulating mutations outside of the target sequence, thereby creating a new local RNA secondary structure that presumably excluded RISC. These results demonstrate conclusively that any effective RNAi-based antiviral therapy must compensate for the evolutionary potential of the pathogen.

source: Antiviral RNAi therapy: emerging approaches for hitting a moving target. Gene Therapy (2006) 13, 532–540

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