Mutational robustness in ribozyme quasispecies

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The aim of the work is to better understand why viral populations under mutagenic pressures can often develop resistant to mutagenic drugs rendering antiviral treatments ineffective.To better understand the molecular underpinning of the extended time to extinction exhibited by populations evolving under mutagenized environmental pressure, during the second FY, I finished measuring fitness values, population sizes with two methods, and to be conservative I redraw the networks after removing single sequences potentially attributable to sequencing errors, cofounding the results.The conservative networks show real genotypic networks for mutagenic treatments, while for the non-mutagenic treatment the complexity of the network largely dropped. There is a clear difference in the amount of genotypic complexity build up in mutagenic treatments. This is key because mutagens have the potential effect of creating evolutionary potential. It is indeed a problem with antiviral therapies: not knowing exactly how much mutagen to add.We also found an important confounding effect of the mutagen used that can help explain the survival of the mutagenized populations (opposite to populations with no mutagen added that went extinct). The increase in population size effect observed, can counteract decreases in size caused by the accumulation of deleterious mutations and/or stochastic effects. These results are provocative and are in process of publication.