April 29, 2025 | Austin, Minn. — Susan Hafenstein, PhD, professor and cryoEM director, and Hyunwook Lee, PhD, research assistant professor at The Hormel Institute, University of Minnesota, have co-authored a paper appearing in Proceedings of the National Academy of Sciences that could help develop more effective vaccines and treatments for animals affected by canine parvovirus (CPV) and has greater implications for how we treat and prevent viruses in humans.
No trip to a pet boarding facility is complete without hearing the question, “Does your dog have its parvo vaccine?”—and for good reason. The virus weakens the immune system, making it harder to fight off infection and, if left untreated, can damage a dog’s intestinal lining and ultimately lead to death. Puppies are especially vulnerable to CPV—in part due to a gap in immunity when puppies still nurse from their mother and when their own immune systems mature, and the way a mother’s milk may interfere with a vaccine’s effectiveness. In addition to domesticated dogs, CPV also affects other species, including foxes, raccoons, and coyotes.
Important as they are, the study’s findings aren’t only of significance for dogs.
“Beyond its clinical relevance for dogs, this research establishes a framework for investigating whether a limited antibody repertoire is a common feature of immune responses to viral infections across other species, including humans,” Dr. Lee said.
“It’s a canine parvovirus and does not infect humans. However, because this virus jumps species, it is important to us,” said Dr. Hafenstein, referring to how CPV arose from a variant of a virus related to feline panleukopenia virus (FPV) in cats. She added that this makes understanding the virus’s mechanisms — and finding ways to keep it in check — all the more important.
In the study, conducted in collaboration with the lab of Colin Parrish, interim director of the Baker Institute of Animal Health under the Cornell University College of Veterinary Medicine, researchers used The Hormel Institute’s cryogenic-sample electron microscopy (cryoEM) technology to investigate how some puppy antibodies respond to and interact with CPV. In doing so, they learned more about how the antibodies’ binding sites (where they attach), binding modes (how they attach), and the mechanisms they use to neutralize the virus.
“Our study provides a view into the ongoing arms race between the canine immune system and CPV’s immune evasion strategies,” Dr. Lee said. “These findings enhance our understanding of fundamental virus-host interactions and pave the way for improving current vaccines and treatments for infected animals. Additionally, the antibodies identified by Parrish’s group could serve as valuable tools for therapeutic or diagnostic applications, while a deeper understanding of virus-host interactions may inform the development of more effective vaccines.”
Other findings from the study include:
- The number of antibodies created after CPV infection in puppies is surprisingly targeted, with only two to three dominant antibodies rather than the dozens or hundreds that immunologists or veterinarians would typically expect. All these antibodies block the receptors the virus uses to bind to host cells and spread the infection, but with varying efficacy. This pattern suggests an evolutionary equilibrium: the virus adapts to persist, while the host minimizes its damage.
- Two of the three monoclonal antibodies shared the same heavy chain and had closely related light chains—two major components of an antibody that play a role in binding to a virus. The antibodies’ binding sites and modes were remarkably similar, but they exhibited significantly different binding affinities for CPV, providing a clear example of affinity maturation—or a growth in the strength of a binding affinity over time—in the host’s adaptive immune system.
- Surprisingly, a structurally equivalent antibody was also found in a different dog used in the researchers’ previous study of polyclonal antibody response to CPV, binding to the same site and exhibiting the same binding mode. This finding highlights the immune system’s tendency to target specific regions of the virus.
You can read the paper here: https://doi.org/10.1073/pnas.2423460122
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Founded in 1942 by The Hormel Foundation, The Hormel Institute, University of Minnesota, makes scientific advancements that enhance wellbeing and extend human life. For more than 80 years, we have pursued our mission to conduct research and provide education in the biological sciences with applications in medicine and agriculture. A part of the University of Minnesota's Research and Innovation Office, The Hormel Institute partners with the region's leading biomedical research facilities, including Mayo Clinic.