Pathogenesis of the most recent variant of canine parvovirus: (CPV-2B)

Canine parvovirus arose in the late 1970's as a highly infectious viral infection of wild and domestic canids. The origin of CPV-2 is unknown, but genetic analysis suggests it arose from a closely related virus infecting other carnivores. The original virus (CPV-2) appeared to survive for only about 2 years. Variant strains of CPV emerged in 1980 (CPV-2a) and 1984 (CPV-2b) and appear to be the prevalent subtypes now circulating in the dog population worldwide. In vitro and in vivo host ranges are complex and poorly defined. CPV-2 replicates in vitro within both feline and canine peripheral blood mononuclear cells, but does not appear to replicate in the cat. In contrast, CPV-2a, -2b replicate efficiently in the cat. Evidence from field observations and limited laboratory study also suggests that the most recent CPV variants are more virulent for dogs than the original CPV-2. Further delineation of the dog response to CPV, as well as differences in the response to each virus strain, is important to understanding the nature of the selective pressures which have allowed the most recent strains of CPV to survive, as well as any mechanisms of increased virulence or host range extension.; The pathogenesis of CPV-2 has been extensively studied; however, studies on the pathogenesis of CPV-2b have not been reported. Here we report studies on the pathogenesis of CPV-2b utilizing pathologic and virologic methods. Strand specific in situ hybridization was also utilized to further define sites of viral replication. Monoclonal antibodies against canine lymphocyte surface proteins were utilized to identify cell phenotypes which support viral replication.; The overall pathogenesis of CPV-2 and CPV-2b was similar; however, differences were found in the kinetics, magnitude and duration of tissue viral growth and serum viremia during the initial week of infection. The kinetics of fecal shedding and antibody response also differed. Both CD8 and B lymphocytes supported growth of CPV-2b. These findings support further adaptation of CPV to the dog and suggest a mechanism of selective adaptation and increased virulence. They also serve as a basis for more thorough characterization of the feline host response to CPV-2 and -2b.