Isolation and Molecular Characterization of Canine and Feline Parvovirus Strains - An Updated Review

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چکیده

Canine parvovirus belongs to the genus Protoparvovirus, family Parvoviridae. The virion is non-enveloped having icosahedral symmetry of 26nm diameter. It has a single stranded negative sense genome of 5.2 kb in length. This single-stranded virus has a DNA genome and use cellular replication machinery, their rate of nucleotide substitution is closer to that of RNA viruses than to that of double-stranded DNA viruses. Phylogenetic analysis showed that all CPV isolates descended from a single ancestor which emerged during mid-1970s and were which was closely related to the long-known feline panleukopenia virus (FPV) that infected cats, mink, and raccoons but not dogs or cultured dog cells [3]. FPV and CPV differ only by 0.5% in their DNA sequences. Inspite of their similarity, CPV-2 was not able to replicate in cat cells. FPV is not the only parvovirus species which infects cats, in addition to MEV, the new variants of canine parvovirus, CPV-2a, 2b and 2c have also penetrated the feline host-range, and they are able to infect and replicate in cats, causing diseases indistinguishable from feline panleukopenia [4]. CPV comprises of two open reading frames, one codes for structural proteins VP1 and VP2 while the other codes for non-structural proteins NS1 and NS2. VP3 is a capsid protein which is formed by proteolytic cleavage of VP2 capsid protein. The VP2 is the major capsid protein and plays an important role in determining the antigenicity and the host range of CPV. In 1978, CPV-2 emerged as a cause of a new disease in dogs throughout the world. The first documentation of the virus as CPV-2 was done in Canada [1]. Canine parvovirus (CPV) and feline panleukopenia virus (FPV) capsids bind to the transferrin receptors (TfRs) of their hosts and use these receptors to infect cells. The binding is partially host specific, as FPV binds only to the feline TfR, while CPV binds to both the canine and feline TfRs [5].

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تاریخ انتشار 2016