Antiviral drugs that lead RNA viruses to produce genetic mutations so fast that they cannot remove deleterious ones may be viable, but also present unknown risks to the host, argues a new SciencePerspective ➡
Viruses depend on the host cell to carry out much of their replication, with each offering only a few virus-specific targets for the development of antiviral therapies. This makes the development of broadly active antivirals difficult to conceptualize. Numerous RNA viruses—including severe acute respiratory syndrome coronavirus 2 , Zika virus, and Chikungunya virus—have led to recent epidemics, highlighting the need for effective antiviral drugs that can be enlisted quickly.
The genome size of an organism is inversely related to the error rate during replication, and this holds true for small RNA viruses with genomes of 7 to 30 kb . For RNA viruses, this translates into one nucleotide substitution for every two to three genomes synthesized. Most mutations are deleterious, but a subset of mutations will give rise to potentially useful phenotypic diversity, which may undergo selection.
The strategy for increasing the rate of new mutations in RNA viruses is to design ribonucleoside analogs that can be metabolized to ribonucleoside triphosphates in cells and then be incorporated into the viral genome during viral RNA synthesis. The design of the analog allows the base portion of the ribonucleotide to base pair ambiguously during subsequent RNA synthesis.
The first ribonucleoside analog that was identified as capable of inducing mutations in an RNA virus was the purine analog ribavirin, which forms base pairs as either adenosine or guanosine when used at high concentrations in human cells in vitro (
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