Population genetic tests suggest that the epidemiologies of JCV and BKV are strikingly different
The JCV and BKV viruses have been used as markers for the study of human evolution by assuming that these viruses coevolved with their host. However, it is currently unclear whether the details of the population expansion of these viruses and humans agree. To study this in more detail, large numbers of complete genomes were used for population genetic tests to detect evidence for population expansion. Relative to the neutral expectation of no selective forces and no demographic changes, the JCV data set contained a striking excess of synonymous and non-synonymous mutations that occur only once in the data set. The same was found for non-synonymous mutations of BKV, but not at all for synonymous mutations of BKV. The different frequency spectra of mutations in JCV and BKV do not result from the inclusion of patients with clinical symptoms associated with BKV and JCV, such as nephropathy or progressive multifocal leucoencefalopathy, nor from the different numbers of genomes available for JCV and BKV. Instead, the distribution of unique mutations and population genetic models that use older mutation classes indicate a striking difference of the historical demographies of JCV and BKV with only the former virus exhibiting the evidence of demographic expansion. Our analyses expand on recent population genetic analyses that document a global population expansion of JCV by taking into account the impact of deleterious mutations and by comparing both human viruses. The striking difference between the demographics of BKV and JCV suggests that important aspects of their epidemiology remain to be discovered.
|Keywords||Deleterious mutations, Demography, Fu and Li's D, Polyomavirus, Population expansion|
|Persistent URL||dx.doi.org/10.1016/j.meegid.2009.04.007, hdl.handle.net/1765/28536|
Mes, T.H.M, van Doornum, G.J.J, & Schutten, M. (2010). Population genetic tests suggest that the epidemiologies of JCV and BKV are strikingly different. Infection, Genetics and Evolution, 10(3), 397–403. doi:10.1016/j.meegid.2009.04.007