Ultraviolet light in the UVC range is a commonly used disinfectant to control viruses in clinical settings and water treatment. However, it is currently unknown whether human viral pathogens may develop resistance to such stressor. Here, we investigate the adaptation of an enteric pathogen, human echovirus 11, to disinfection by UVC, and characterized the underlying phenotypic and genotypic changes. Repeated exposure to UVC lead to a reduction in the UVC inactivation rate of approximately 15 per cent compared to that of the wild-type and the control populations. Time-series next-generation sequencing data revealed that this adaptation to UVC was accompanied by a decrease in the virus mutation rate. The inactivation efficiency of UVC was additionally compromised by a shift from first-order to biphasic inactivation kinetics, a form of ‘viral persistence’ present in the UVC resistant and control populations. Importantly, populations with biphasic inactivation kinetics also exhibited resistance to ribavirin, an antiviral drug that, as UVC, interferes with the viral replication. Overall, the ability of echovirus 11 to adapt to UVC is limited, but it may have relevant consequences for disinfection in clinical settings and water treatment plants.

Influenza virus inflicts a heavy death toll annually and resistance to existing antiviral drugs has generated interest in the development of agents with novel mechanisms of action. Favipiravir is an antiviral drug that acts by increasing the genome-wide mutation rate of influenza A virus (IAV). Potential synergistic benefits of combining oseltamivir and favipiravir have been demonstrated in animal models of influenza, but the population-level effects of combining the drugs are unknown. In order to elucidate the underlying evolutionary processes at play, we performed genome-wide sequencing of IAV experimental populations subjected to serial passaging in vitro under a combined protocol of oseltamivir and favipiravir. We describe the interplay between mutation, selection, and genetic drift that ultimately culminates in population extinction. In particular, selective sweeps around oseltamivir resistance mutations reduce genome-wide variation while deleterious mutations hitchhike to fixation given the increased mutational load generated by favipiravir. This latter effect reduces viral fitness and accelerates extinction compared with IAV populations treated with favipiravir alone, but risks spreading both established and newly emerging mutations, including possible drug resistance mutations, if transmission occurs before the viral populations are eradicated.

Levels of nucleotide diversity vary greatly across the genomes of most species owing to multiple factors. These include variation in the underlying mutation rates, as well as the effects of both direct and linked selection. Fundamental to interpreting the relative importance of these forces is the common observation of a strong positive correlation between nucleotide diversity and recombination rate. While indeed observed in humans, the interpretation of this pattern has been difficult in the absence of high-quality polymorphism data and recombination maps in closely related species. Here, we characterize genetic features driving nucleotide diversity in Western chimpanzees using a recently generated whole genome polymorphism data set. Our results suggest that recombination rate is the primary predictor of nucleotide variation with a strongly positive correlation. In addition, telomeric distance, regional GC-content, and regional CpG-island content are strongly negatively correlated with variation. These results are compared with humans, with both similarities and differences interpreted in the light of the estimated effective population sizes of the two species as well as their strongly differing recent demographic histories.