MERS-CoV spillover at the camel-human interface

Gytis Dudas; Luiz Max Carvalho; Andrew Rambaut; Trevor Bedford; Ali M. Somily; Mazin Barry; Sarah S. Al Subaie; Abdulaziz A. BinSaeed; Fahad A. Alzamil; Waleed Zaher; Theeb Al Qahtani; Khaldoon Al Jerian; Scott J.N. McNabb; Imad A. Al-Jahdali; Ahmed M. Alotaibi; Nahid A. Batarfi; Matthew Cotten; Simon J. Watson; Spela Binter; Paul Kellam

Owing to these findings, we performed a sensitivity analysis in which we partitioned the MERS-CoV genome into two fragments and identified human outbreak clusters within each fragment. We find strong similarity in the grouping of human cases into outbreak clusters between fragments ( Figure 4A ). Between the two trees in figure 4B four (out of 54) 'human' clades are expanded where either singleton introductions or two-taxon clades in fragment 2 join other clades in fragment 1. For the reverse comparison there are five 'human' clades (out of 53) in fragment 2 that are expanded. All such clades have low divergence (figure 4B) and thus incongruences in human clades are more likely to be caused by differences in deme assignment rather than actual recombination. And while we observe evidence of distinct phylogenetic trees from different parts of the MERS-CoV genome ( Figure 4B ), human clades are minimally affected and large portions of the posterior probability density in both parts of the genome are concentrated in shared clades ( Figure S12 ). Additionally, we observe the same source-sink dynamics between camel and human populations in trees constructed from separate genomic fragments as were observed in the original full genome tree (Figures 1, 4B ).