Hepatitis C virus occupies a special niche in virology and is the cause of considerable morbidity and mortality worldwide. 50-80% of infected individuals become chronically infected. This RNA virus practices ¿genomic origami¿, condensing the necessary prerequisites for replication, translation and perpetuation of viral infections into a 9.6kb genome. The very significant degree of heterogeneity is generated in large measure by the error prone RNA replicase generating quasispecies. This genomic quasispecies exhibits a spectrum of viral fitness that potentiates viral persistence and protects viral families against future purifying selection. Our investigations into quasispecies have yield insights into viral population dynamics during chronic hepatitis C infection, and cytotoxic T cell immunity and how treatment modulates the quasispecies qualitatively and quantitatively. We now know that continuous immune surveillance can create bottle necks during transmission to new hosts and viral adaption can leave ¿genomic footprints¿ giving a clearer picture of quasispecies evolution. The functional consequences of quasispecies is such that HCV has the capacity to produce mutants that have varying degrees of resistance to temporally unique positive selection pressures, to have mutant spectra that are associated with resistant to novel anti-virals, even in untreated individuals. The phenomenon of quasispecies endows hepatitis C with an almost endless capacity to mutate and provides this virus with a degree of ¿future proofing¿ not found in many biota.