Predicting the emergence of novel infectious diseases requires an understanding of how pathogens infect and efficiently spread in alternative naïve hosts. A pathogen's ability to adapt to a new host (i.e. host shift) oftentimes is constrained by host phylogeny, due to limits in the molecular mechanisms available to overcome host-specific immune defences (Longdon et al., 2014). Some pathogens, such as RNA viruses, however, have a propensity to jump hosts due to rapid mutation rates. For example, canine distemper virus (CDV) infects a broad range of terrestrial carnivores, as well as noncarnivore species worldwide, with a host range that is distributed across 5 orders and 22 families (Beineke et al., 2015). In 1993-1994, a severe CDV outbreak infected multiple carnivore host species in Serengeti National Park, causing widespread mortality and the subsequent decline of the African lion (Panthera leo) population (Roelke-Parker et al., 1996). While previous studies established domestic dogs (Canis lupus familiaris) as the disease reservoir, the precise route of transmission to lions remained a mystery, and a number of wild carnivore species could have facilitated viral evolution and spread. In this issue of Molecular Ecology, Weckworth et al. (2020) used whole-genome viral sequences obtained from four carnivore species during the CDV outbreak, in combination with epidemiological data, to illuminate the pathway and evolutionary mechanisms leading to disease emergence in Serengeti lions.
Keywords: canine distemper virus; disease transmission; epidemiology; morbilliviruses; pathogen spillover; phylodynamics.
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