Above is a schematic of the single-particle tracking binding assay used in the study.

Canine parvovirus (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, according to an early study by Chinese researchers.

But how do such viruses jump from one species to another, and from wild to domesticated animals, and vice versa? A new study offers some clues.

Researchers from Cornell University (Cornell) have identified a mutation in CPV that can profoundly alter transferrin receptor (TfR) binding and infectivity of the virus.

The study was published online in the Journal of Virology on Feb. 17.

The researchers contend 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. Another key factor in CPV’s infectivity is adhesion strengthening during TfR binding.

“There’s an initial attachment, which is probably relatively weak,” said Colin R. Parrish, PhD, the John M. Olin Professor of Virology and director of the Baker Institute for Animal Health at Cornell, and one of the study’s authors. “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.

“We think that the second event, this structural interaction that occurs in a small proportion of the binding cases, seems to be critical,” Parrish 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.”

Photo credit: Cornell University