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      Canine Parvovirus (CPV) Vaccination: Comparison of Neutralizing Antibody Responses in Pups after Inoculation with CPV2 or CPV2b Modified Live Virus Vaccine

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          ABSTRACT

          Canine parvovirus type 2 (CPV2) emerged in 1978 as causative agent of a new disease of dogs. New antigenic variants (biotypes), designated CPV2a and CPV2b, became widespread during 1979 to 1980 and 1984, respectively. At the present time the original CPV2 has disappeared in the dog population and has been replaced by the two new viruses. In the present study the comparison of neutralizing antibody titers in two groups of pups (18 pups in each group) inoculated with CPV2 and CPV2b modified live virus vaccines is reported. Using the hemagglutination inhibition (HI) test, relevant differences between antibody titers, against either the homologous or the heterologous virus, were not constantly observed. Using the neutralization (Nt) test, however, the pups inoculated with CPV2 had antibody titers which were approximately 30 times higher to the homologous virus (mean, 4,732) than to the heterologous virus (CPV2b) (mean, 162). The results of these experiments support two conclusions: (i) the HI test may not always accurately evaluate the true immune status of dogs with respect to CPV, and (ii) dogs inoculated with CPV2 vaccine develop relatively low Nt antibody titers against the heterologous virus (CPV2b). These data may suggest an advantage for new vaccines, considering that most presently licensed vaccines are produced with CPV2, which no longer exists in the dog population.

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          Most cited references6

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          Antigenic structure and variation of canine parvovirus type-2, feline panleukopenia virus, and mink enteritis virus.

          The antigenic structure and variation of canine parvovirus type-2 (CPV), feline panleukopenia virus (FPV), mink enteritis virus (MEV), and a closely related virus of raccoons (RPV) was investigated using a panel of 13 monoclonal antibodies (mAb) formed against CPV and 8 mAb formed against FPV. Each mAb both neutralized and inhibited the hemagglutination of the homologous virus. All mAb tested immunoprecipitated the two capsid proteins. Five mAb were specific for the CPV isolates and one reacted with the FPV, MEV, and RV isolates, but not the CPV. Another mAb reacted only with certain FPV and MEV isolates. The remaining 14 mAb reacted with most parvoviral isolates from the four animal species. Antigenic variation was observed both within and between the parvovirus isolates from each species. The 12 MEV isolates could be grouped into three antigenic types based on their reactivity with the panel of mAb. Antigenic variants of either CPV or FPV were readily selected with several mAb. Analysis of these variant viruses by direct serological tests and competition radioimmune assays between different mAb revealed that the capsid surface contained at least two determinants, each being comprised of many different but overlapping epitopes.
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            Characterization of the feline host range and a specific epitope of feline panleukopenia virus.

            The feline parvovirus subgroup is comprised of viruses isolated from various carnivores, including the dog, cat, mink, raccoon, Arctic fox, and raccoon dog. Those viruses are > 98% identical in their DNA sequences and are very similar antigenically. We have shown that although canine parvovirus (CPV) replicates in numerous feline cell lines in vitro it does not infect cats after parenteral inoculation (U. Truyen and C. R. Parrish, (1992) J. Virol. 66, 5399-5408). Here we use recombination mapping to locate some viral determinants required for feline host range, and show that the ability to replicate in cats was determined by the right-hand 45% of the genome, most likely a function of the capsid protein gene. Efficient replication in the cat appeared to require feline panleukopenia virus sequences from both ends of the VP2 molecule, which contained differences of VP2 amino acid residues 80, 564, and 568. The difference at amino acid 80 was also associated with expression of an FPV-specific antigenic epitope. The differences which affected the feline host range were located in a region of the capsid structure where three VP2 molecules interact, and the mutations gave rise to changes in the conformation of loops of the three adjoining VP2 monomers. The mechanism(s) of the in vivo feline host range restriction were not defined, and we were unable to show in vitro inhibition of virus infectivity by feline serum components or erythrocytes.
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              AN ENTERIC DISEASE OF DOGS RESEMBLING FELINE PANLEUCOPAENIA

              W.R. KELLY (1978)
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                Author and article information

                Journal
                Clinical Diagnostic Laboratory Immunology
                Clin. Diagn. Lab. Immunol.
                American Society for Microbiology
                1098-6588
                1071-412X
                May 01 2001
                May 01 2001
                : 8
                : 3
                : 612-615
                Affiliations
                [1 ] Department of Health and Animal Well-Being, Faculty of Veterinary Medicine, University of Bari, Bari, Italy,1 and
                [2 ] James A. Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, New York2
                Article
                10.1128/CDLI.8.3.612-615.2001
                96110
                11329467
                80f771a2-756c-44ba-9e86-f3e3cff554e2
                © 2001
                History

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