HOW THE DISTEMPER VIRUS JUMPS TO OTHER SPECIES.

Distemper has been noted to affect tigers,lions and some bears .See(http://veterinarymedicineechbeebolanle-ojuri.blogspot.com.ng/2016/04/distemper-virus-and-tigers.html). Canine distemper, a viral disease that has infected the lions of Tanzania's Serengeti National Park, appears to be spread by multiple animal species, according to a study published by a transcontinental team of scientists. In 1994, a mysterious neurological ailment wiped out 30-percent of the lion population in the Serengeti, one of the largest wildlife regions in the world. Scientists determined it was canine distemper, a disease previously thought to infect only dogs, coyotes and a small number of other mammals. Evidence suggested the lions had contracted the virus from dogs living in villages and settlements nearby. A domestic dog vaccination campaign was launched to curb the infection's spread. It worked--among dogs, at least. After analyzing three decades of blood serum data collected from lions and domestic dogs, the researchers discovered that the virus continues to circulate in the lion population while significantly declining among dogs. A new research by researchers in Cornell university have shown how the virus jumps to other species, a key mutation in the protein shell of canine parvovirus -- a single amino acid substitution -- plays a major role in the virus' ability to infect hosts of different species. Canine parvovirus, or CPV, emerged as a deadly threat to dogs in the late 1970s, most likely the result of the direct transfer of feline panleukopenia or a similar virus from domesticated cats. CPV has since spread to wild forest-dwelling animals, including raccoons, and the transfer of the virus from domesticated to wild carnivores has been something of a mystery. Colin Parrish, the John M. Olin Professor of Virology and director of the Baker Institute for Animal Health at Cornell University co-authored a research paper, published in the Journal of Virology, with Susan Daniel, associate professor in Cornell's Robert Frederick Smith School of Chemical and Biomolecular Engineering, which contends that a key mutation in the protein shell of CPV -- a single amino acid substitution -- plays a major role in the virus' ability to infect hosts of different species. There's an initial attachment, which is probably relatively weak," he said. "The thing just grabs on and holds on a little bit, sort of like using your fingertips. And then it looks like there's a second attachment that is much stronger, where it's like you grab on and hold on with both hands and won't let go." The second event, is structural interaction that occurs in a small proportion of the binding cases, seems to be critical," he said. "We think that it actually causes a change in the virus, that it triggers a small shift in the virus that actually makes it able to infect successfully." One of Daniel's specialties is the investigation of chemically patterned surfaces that interact with soft matter, including biological materials such as cells, viruses, proteins and lipids. Her lab has pioneered a method called single-particle tracking -- placing artificial cell membranes into microfluidics devices, fabricated at the CNF, to study the effect of single virus particles on a variety of membrane host receptors, in this case from both dogs and raccoons.