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Does the Middle East Respiratory Syndrome coronavirus (MERS-CoV) recombine?

Gytis Dudas1 and Andrew Rambaut1,2,3

1Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK, 2Fogarty International Center, National Institutes of Health, Bethesda, MD, USA, 3Centre for Immunology, Infection and Evolution at the University of Edinburgh, Edinburgh, UK

Quick summary

Very likely, yes. This repo is what I've been up to lately and is nearly finished. Most/all of the work has been done and it shows the presence of the classical recombination triad in the MERS genome: excessive homoplasies, decay of linkage disequilibrium and the presence of alternative topologies.

Done:

  • GARD analyses. Show that the MERS genome has well-supported alternative tree topologies and some degree of rate heterogeneity.
  • LDhat analyses. Permutation tests for recombination in LDhat appear quite robust to temporal sampling and indicate LD decay. Some other tests don't do so well.
  • Homoplasy analyses. Ancestral sequence reconstruction using ClonalFrameML indicates excessive numbers of homoplasies in the MERS genome.
  • Host-polymorphism association analysis. Present data do not show the presence of "human" or "camel" alleles, but are also too poorly sampled to address the question in great detail.
  • Homoplasy rates integrating over possible tree topologies. Shows almost identical results to ML analysis.
  • Marginal likelihood estimates of models including/excluding rate heterogeneity and/or alternative tree topologies. Mostly done and appears to support a model with rate heterogeneity alone, which is not surprising given the overall appearance of recombination and the cost of the number of parameters introduced by another phylogenetic tree.
  • Manuscript.

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