ABSTRACT
Canine parvovirus (CPV), a highly contagious virus causing acute gastroenteritis in domestic dogs, is prevalent all over the world, mainly because this virus can survive in adverse environmental conditions for a long time [1]. Natural CPV-2 infection has been reported in domestic dogs, bush dogs, cats, coyotes, bears, and wolves. The disease is clinically characterized by severe vomiting, pyrexia, anorexia, and diarrhea leading to fatal dehydration as well as myocarditis particularly in young pups. CPV-2 is a nonenveloped, single-stranded DNA virus belonging to the Parvoviridae family and genus Parvovirus, along with feline panleukopenia virus (FPLV) and other parvoviruses of carnivores [2]. A wide range of species are affected by viruses of the Parvoviridae family; however, CPV-2 does not cross species lines [2]. After its emergence in the 1970s, CPV-2 underwent a rapid evolution, and within a few years, new antigenic types emerged at regular intervals, termed CPV-2a in 1978, CPV-2b in 1984, and CPV-2c in 1997 and completely replaced the original CPV-2. Presently, the original CPV-2 type no longer circulates in the dog population, whereas CPV-2a and CPV-2b types are distributed worldwide; now, CPV-2a and CPV-2b types have further undergone several mutations that produced variants of CPV-2a (New CPV-2a) and CPV-2b (New CPV-2b). Mutations affecting the VP2 gene of CPV have been responsible for the evolution of different antigenic variants. Sequence analysis of the VP2 gene of the virus and subsequent characterization is important for molecular epidemiology of CPV [3].
