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Colin R. Parrish, Ph.D.

John M. Olin Professor of Virology

Dr. Colin Parrish’s research focuses on certain viruses of dogs, cats, and horses that still cause a significant number of illnesses and deaths despite the availability of effective vaccines.  Each of these viruses also has a history of moving from one species of animal into another and causing an epidemic, and Dr. Parrish’s lab is working on understanding the principles behind how this emergence in new hosts works. Dr. Parrish’s current projects explore the evolution of canine parvovirus, ways to predict outbreaks of new and old viruses, and approaches that may be used for eradicating canine influenza, all efforts with the potential for a significant impact on the health of dogs, cats, horses, and wildlife. An animal lover, Dr. Parrish and his family share their home with five cats and three dogs.

Canine parvovirus first appeared in 1978 in a global pandemic that killed dogs by the hundreds of thousands. Although it evolved from feline panleukopenia virus, which is specific to cats, canine parvovirus now appears to infect most carnivores worldwide (members of the Order Carnivora), including carnivores native to North America, many of which are critically endangered. Genetic evidence indicates it all started when a single feline panleukopenia virus mutated and gained the ability to attach to receptors on the cells of dogs. Dr. Parrish and his colleagues are studying how the virus has evolved since 1978, tracking the spread of new variants of the virus and the ways they differ from their predecessors. This natural variation in the virus over time could make problems for vaccination efforts, so they’re also taking a close look at the structure of the viral surface and how the virus attaches to host antibodies and to the receptors on the surface of dog cells. This will allow them to determine whether the vaccine for parvovirus is still a good match for the strains that are in circulation, and if the vaccine and the virus are mismatched, it may be time to update the parvovirus vaccine.

On a related vein, Dr. Parrish’s laboratory is using molecular information like this to predict and to prevent the emergence of new epidemics of viral disease. Zoonoses are diseases that jump from animals to human populations (like the pandemic influenza strain of 1918, Ebola, and rabies). Zoonotic diseases are becoming increasingly common, most likely as a result of increasing intensification of agriculture and human encroachment on wild areas, and their ability to cross international borders easily makes them a global problem. Working with an international team of scientists, Dr. Parrish’s lab is studying the properties of host-jumping animal viruses and receptors on host cells and putting this information into the context of human and animal exposure to viruses, transmission, global travel, and other factors, in an attempt to understand the fundamental principles behind the emergence of new diseases. By weaving all this information together into a mathematical model, it may also be possible to identify viruses in animals that might someday cross over to humans, allowing public health authorities to put interventions in place to stop that from happening.

Influenza is one virus that’s particularly well-known for crossing between different species. Dr. Parrish’s lab is studying H3N8, a flu strain that jumped from horses into dogs in 1999, which lead to a widespread outbreak in the following few years, but today the virus seems to be maintained only in dogs at a handful of large animal shelters. It’s not well understood why, after 14 years of continuous circulation, “dog flu” hasn’t spread widely among the general dog population. Dr. Parrish and his colleagues are studying the genomes of the virus and modeling the rate at which it moves from dog to dog to determine why H3N8 has died out in many locations and how control measures might be used to further limit spread. Their early results show the virus is not very transmissible, and that to maintain disease in a population each infected dog would have to have contact with two or three other dogs during the short period when the animal sheds significant numbers of viruses. These results indicate that control measures should be possible to eradicate “dog flu”, an accomplishment that would represent a rare achievement in animal health.


1. Lyi SM, Tan MJ, Parrish CR. (2014). Parvovirus particles and movement in the cellular cytoplasm and effects of the cytoskeleton. Virology, 456-457:342-52. Abstract.

2. Löfling J1, Michael Lyi S, Parrish CR, Varki A. (2013). Canine and feline parvoviruses preferentially recognize the non-human cell surface sialic acid N-glycolylneuraminic acid. Virology, 25;440(1):89-96. Abstract.

3.  Flanagan ML1, Parrish CR, Cobey S, Glass GE, Bush RM, Leighton TJ. (2012). Anticipating the species jump: surveillance for emerging viral threats. Zoonoses and Public Health, 59(3):155-63. Abstract.

4.  Malik Peiris JS, Parrish CR. (2011). Emerging viruses. Current Opinion in Virology, 1(6):617-9. Abstract.

5.  Allison AB1, Kohler DJ, Fox KA, Brown JD, Gerhold RW, Shearn-Bochsler VI, Dubovi EJ, Parrish CR, Holmes EC. (2013). Frequent cross-species transmission of parvoviruses among diverse carnivore hosts. Journal of Virology, 87(4):2342-7.

6.  Markovich JE1, Stucker KM, Carr AH, Harbison CE, Scarlett JM, Parrish CR. (2012). Effects of canine parvovirus strain variations on diagnostic test results and clinical management of enteritis in dogs. JAVMA - Journal of the American Veterinary Medical Association, 1;241(1):66-72. Abstract.

7.  Kaelber JT1, Demogines A, Harbison CE, Allison AB, Goodman LB, Ortega AN, Sawyer SL, Parrish CR. (2012). Evolutionary reconstructions of the transferrin receptor of Caniforms supports canine parvovirus being a re-emerged and not a novel pathogen in dogs. PLOS Pathogens, 8(5):e1002666.

8.  Cureton DK1, Harbison CE, Cocucci E, Parrish CR, Kirchhausen T. (2012). Limited transferrin receptor clustering allows rapid diffusion of canine parvovirus into clathrin endocytic structures. Journal of Virology, 86(9):5330-40.

9.  Stucker KM1, Pagan I, Cifuente JO, Kaelber JT, Lillie TD, Hafenstein S, Holmes EC, Parrish CR. (2012). The role of evolutionary intermediates in the host adaptation of canine parvovirus. Journal of Virology, 86(3):1514-21.

10.  Allison AB1, Harbison CE, Pagan I, Stucker KM, Kaelber JT, Brown JD, Ruder MG, Keel MK, Dubovi EJ, Holmes EC, Parrish CR. (2012). Role of multiple hosts in the cross-species transmission and emergence of a pandemic parvovirus. Journal of Virology, 86(2):865-72.

11.  Kim JW1, Lyi SM, Parrish CR, Parker JS. (2011). A proapoptotic peptide derived from reovirus outer capsid protein {micro}1 has membrane-destabilizing activity. Journal of Virology, 85(4):1507-16.

12.  Hayward JJ1, Dubovi EJ, Scarlett JM, Janeczko S, Holmes EC, Parrish CR. (2010). Microevolution of canine influenza virus in shelters and its molecular epidemiology in the United States. Journal of Virology, 84(24):12636-45.

13.  Hoelzer K1, Parrish CR. (2010). The emergence of parvoviruses of carnivores. Veterinary Research, 41(6):39.

14.  Goodman LB1, Lyi SM, Johnson NC, Cifuente JO, Hafenstein SL, Parrish CR. (2010). Binding site on the transferrin receptor for the parvovirus capsid and effects of altered affinity on cell uptake and infection. Journal of Virology, 84(10):4969-78.

15.  Hoelzer K, Murcia PR, Baillie GJ, Wood JL, Metzger SM, Osterrieder N, Dubovi EJ, Holmes EC, Parrish CR. (2010). Intrahost evolutionary dynamics of canine influenza virus in naive and partially immune dogs. Journal of Virology, 84(10):5329-35.