Abstract
Parvoviruses exploit transferrin receptor type-1 (TfR) for cellular entry in carnivores, and specific interactions are key to control of host range. We show that several key mutations acquired by TfR during the evolution of Caniforms (dogs and related species) modified the interactions with parvovirus capsids by reducing the level of binding. These data, along with signatures of positive selection in the TFRC gene, are consistent with an evolutionary arms race between the TfR of the Caniform clade and parvoviruses. As well as the modifications of amino acid sequence which modify binding, we found that a glycosylation site mutation in the TfR of dogs which provided resistance to the carnivore parvoviruses which were in circulation prior to about 1975 predates the speciation of coyotes and dogs. Because the closely-related black-backed jackal has a TfR similar to their common ancestor and lacks the glycosylation site, reconstructing this mutation into the jackal TfR shows the potency of that site in blocking binding and infection and explains the resistance of dogs until recent times. This alters our understanding of this well-known example of viral emergence by indicating that canine parvovirus emergence likely resulted from the re-adaptation of a parvovirus to the resistant receptor of a former host.
Highlights
The interactions between viral pathogens and their hosts present a longstanding evolutionary challenge for both participants
Because of the recent emergence of Canine parvovirus (CPV), it was previously thought that parvoviruses have been infecting Feliforms and some Caniforms for much longer than they have infected domestic dogs and closely related coyotes and wolves
We examined the apical domain region of the TFRC genes of other Caniform species closely related to domestic dogs, the coyote, black-backed jackal, and bat-eared fox (Figure 1B)
Summary
The interactions between viral pathogens and their hosts present a longstanding evolutionary challenge for both participants. The viruses that exist today have been shaped by a sustained interplay with hosts over long periods of evolutionary time [1]. Much attention has been focused on the evolution of viruses, but less is known about the corresponding variation and selection of relevant host genes. It is clear that pathogen-driven selective pressures can drive genetic change in the host genes that control susceptibility and disease progression. The analysis of these evolutionary interplays helps elucidate the factors that control viral emergence, defined here as the establishment of an existing virus in a novel host species
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