Since its emergence in 2012, MERS-CoV has remained an endemic zoonotic pathogen in the Arabian Peninsula; most human cases come from the Kingdom of Saudi Arabia (KSA), where dromedary camels serve as the primary reservoir1. MERS-CoV can be classified by sequence analysis into three clades (clades A, B and C), each of which branches into more granular lineages that are continuing to evolve2. In addition to these lineages, circulating recombinant forms have emerged; there is limited knowledge on how the observed genomic diversity translates to specific viral traits3. To date, over 2,600 laboratory-confirmed human cases have been reported globally, with a crude case–fatality ratio of approximately 37%. MERS-CoV spreads in strikingly different ways across regions. In Africa, clade C dominates, but human Middle East respiratory syndrome (MERS) has so far not been officially reported — although there is increasing evidence that human infection is taking place4. In the Middle East, clade B drives frequent camel-to-human MERS-CoV infections, which intensify during calving season. Although laboratory evidence suggests clade differences in relation to virulence and infectivity, it remains unclear why these patterns diverge.