Canine parvovirus: An update on variants

Canine parvovirus: An update on variants

A review of what's happening with canine parvovirus in the United States.
source-image
Aug 01, 2009

Q: Please review what's happening with canine parvovirus in the United States.

A: Dr. Sanjay Kapil gave an excellent lecture on "Canine parvovirus variants circulating in the United States (2006-2008)" at this year's American College of Veterinary Internal Medicine Forum in Montreal, Canada. Here are some relevant points from it:

Canine parvovirus (CPV) emerged as a new pathogen of dogs in the 1970s. Today, it is the most common viral disease of dogs. There are two canine parvoviruses: canine parvovirus-1 (minute virus of canines) and canine parvovirus-2, the primary cause of puppy enteritis, morbidity and mortality. CPV-1 and CPV-2 are antigenically and genetically different.

Canine parvovirus contains a single-stranded DNA of about 5,000 bases. This small virus has only major proteins, viral protein 1 (VP1) and viral protein 2 (VP2). CPV is a non-enveloped virus that is resistant to lipid solvents, temperature and pH changes. Due to a compact DNA genome, parvovirus has high physical resistance.

CPV-2 can survive in the kennel environment for months or years. If the kennel is not properly cleaned, the virus can be transmitted to the next batch of naïve puppies.

Canine parvovirus genome tends to mutate at critical amino acids (about 10 residues) of VP-2 capsid protein.

Evolution of CPV-2 in the last 30 years

A CPV-2 pandemic began in 1977. It was associated with high mortality due to hemorrhagic diarrhea and myocarditis. The virus probably originated from a carnivore parvovirus (feline panleukopenia, mink parvovirus or blue fox parvovirus).

These viruses have high genetic similarity (99 percent). However, they have biological differences, such as differences in the suitable pH for maximum hemagglutination activity. For example, based on a recent study, feline parvovirus interacts with transferrin receptor at a pH of 6.5. However, a recent CPV-2c can interact with transferrin from pH (3-8).

These genetically closely related viruses have acquired host-range differences due to single-point mutations on the VP2 protein. The prototype CPV-2 isolates did not infect cats but could grow in feline cell lines such as Crandall Reese feline kidney (CRFK) cell line. CPV-2 soon acquired the ability to infect cats by point mutations that broadened the host range.

By 1982, a genetic variant emerged that had amino-acid changes at positions 87, 101, 300, 305 and 555 of the VP2 protein. This genetic variant was designated CPV-2a to distinguish it from the original CPV-2. CPV-2a had acquired the ability to infect cats, and it had isoleucine instead of valine at position 555 of the VP2 protein.

In 1985, another genetic variant designated CPV-2b emerged, spreading worldwide. It is the major genotype of CPV-2 in the United States. In 2000, Dr. Buonavoglia from Bari, Italy, reported a new genotype of CPV-2 that had glutamic acid at position 426 of the VP2. This virus is the second major genotype of CPV-2 in the United States. CPV-2c has now been documented on all continents except Australia. In addition to natural evolution of CPV-2, there are other mechanisms of antigenic and genetic changes in the current CPV-2 isolates.