Emerging infectious diseases constitute some of the most pressing problems for both human and domestic animal health, and biodiversity conservation. Currently it is not clear whether the removal of past constraints on geographical distribution and transmission possibilities for pathogens alone are sufficient to give rise to novel host–pathogen combinations, or whether pathogen evolution is also generally required for establishment in novel hosts. Canine distemper virus (CDV) is a morbillivirus that is prevalent in the world dog population and poses an important conservation threat to a diverse range of carnivores. We performed an extensive phylogenetic and molecular evolution analysis on complete sequences of all CDV genes to assess the role of selection and recombination in shaping viral genetic diversity and driving the emergence of CDV in non-dog hosts. We tested the specific hypothesis that molecular adaptation at known receptor-binding sites of the haemagglutinin gene is associated with independent instances of the spread of CDV to novel non-dog hosts in the wild. This hypothesis was upheld, providing compelling evidence that repeated evolution at known functional sites (in this case residues 530 and 549 of the haemagglutinin molecule) is associated with multiple independent occurrences of disease emergence in a range of novel host species.
Alex J McCarthy, Marie-Anne Shaw and Simon J Goodman, Pathogen evolution and disease emergence in carnivores Proceedings of the Royal Society B: Biological Sciences” Proc. R. Soc. 22 December 2007 vol. 274 no. 1629 3165-3174