If you've heard of the disease distemper it may be because you had to get your dog vaccinated against it. Dog or canine distemper is caused by a measles-like virus, Canine Distemper Virus, but it doesn't just affect dogs. It is capable of jumping to other species and wiped out about 10% of the world's smallest seals, the Caspian seals. Other carnivores that have taken a big hit from CDV are the Tasmanian tiger and black-footed ferret. It can infect infect lions and hyenas and probably other animals in the wild. So the question of what enables the dog virus to jump to other species is not just an academic question. In many ways it is like the bird flu question. Bird flu is a virus primarily of birds, but on occasion it jumps to other species, including humans. What determines this? The bird flu question has received a lot of attention, although there is no single answer, only tantalizing small pieces of what seems to be a larger puzzle. New work on CDV seems to be revisiting similar ground to the bird flu story:
"The virus needs to bind to a specific receptor on cells in the host in order to infect it," explains lead researcher, PhD student Alex McCarthy, from the University [of Leeds] Faculty of Biological Sciences. "But the sequences of receptors vary between species, so a virus from one species shouldn't be able recognise and infect the cells of other species."By analysing the virus' genetic sequence in both dog and wild carnivore species, the research team were able to prove that two key parts of a CDV protein specifically involved in receptor recognition had evolved during the host jumps, where as the rest of the protein showed very few changes among viruses from different species.
"It was a very satisfying moment when our ideas proved correct," says McCarthy. "The results really screamed out at us. They were so clear- cut, we think it's highly likely that pathogen evolution is a much more general mechanism in cross-species transmission of viruses than anyone imagined." (ScienceDaily)
This sounds pretty familiar. Exactly the same story was being told by flu researchers whose version was that birds had one kind of receptor (α2,3Gal) and humans another (α2,6Gal; see our post here and links therein). Indeed it was such a satisfying story it was believed for more than a decade. But we now know it is more complicated than that (see here and here, etc.). Yes, the receptors undoubtedly play some part, maybe a major part. But there is much more to it and in some cases there may be alternate routes to host specificity for bird flu.
Maybe CDV is very different and the receptor tells the whole story. But I wouldn't count on it. As to whether virus evolution is playing more of a part in CDV "than anyone imagined" I can't say because I don't know the work on that virus well, but if true, it shows both a lack of imagination and unfamiliarity with many other viruses.
On the other hand, scientists (and not just young ones) sometimes make these kinds of exaggerated claims for their work. They are, after all, human.
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Revere,
The 2nd "here" link (/effectmeasure/2007/10/%20flu_biology_receptors_i.php) appears to be broken.
I'm not at all sure about my raccoon dogs (nyctereutes procyonoides), but since they occupy a unique niche between Mustelidae and Canidae I've had them vaccinated. I'm fairly sure they could catch it.
If a disease were tansmitted by fleas, now that would be another matter, because mine NEVER have fleas. Nor does my husky who lives among them. I don't know of any research into this curious phenomenon, and it's a bit off topic, but I thought it might interest you.
The paper also reads:
"Of course other functional adaptation may also be important for, or arise after establishment in new hosts (Webby et al. 2004), as evidenced by the substitutions which modulate virulence in the VEEV and WNV examples."
So other possible causes for host switching are acknowledged even if only in passing. As are other sources of causality:
"The future challenges are to increase our understanding of how these evolutionary processes interact with new selection pressures on pathogens arising from human drivers such as globalization, agricultural intensification and impingement into new habitats, to promote disease emergence. Unifying identification of functional adaptation with molecular estimates of the time of disease emergence events and linking these to known changes in human drivers will likely offer a productive way forward."
When it is on a dinner plate in China.
A dog of any breed, but specially if it is a St. Bernard.
They really love a good St. Bernard with black bean sauce there!