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Characterization of a nonhemagglutinating mutant of canine parvovirus
C R Parrish1, G Burtonboy, L E Carmichael
1James A. Baker Institute for Animal Health, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853.
Abstract:
A nonhemagglutinating mutant of a 1978 isolate of canine parvovirus (CPV) was derived after repeated passages in the NLFK feline kidney cell line. The mutant CPV was antigenically indistinguishable from wild-type virus when tested with 82 monoclonal antibodies, and it replicated in cat and dog cell lines in culture. Sequences of the VP-1 and VP-2 genes revealed two nucleotide and two predicted amino acid sequence differences at 77 and 88 genome map units in the mutant compared to hemagglutinating viruses. One or both of those two mutations must determine the difference in the ability of the virus to agglutinate erythrocytes.
Insights
A canine parvovirus (CPV) mutant lacking hemagglutination was created. Specific gene mutations in the mutant CPV likely explain its inability to agglutinate erythrocytes, impacting viral properties.
Area of Science:
- Veterinary Virology
- Molecular Virology
- Canine and Feline Infectious Diseases
Background:
- Canine parvovirus (CPV) is a highly contagious pathogen affecting dogs.
- Hemagglutination is a key viral property used for classification and understanding host interactions.
- Previous studies have not fully elucidated the genetic basis of CPV hemagglutination.
Purpose of the Study:
- To generate and characterize a nonhemagglutinating mutant of canine parvovirus (CPV).
- To identify the genetic mutations responsible for the loss of hemagglutination in CPV.
- To understand the molecular basis of CPV hemagglutination and its potential impact on viral infectivity.
Main Methods:
- Derivation of a nonhemagglutinating CPV mutant through serial passages in NLFK feline kidney cells.
- Antigenic characterization of the mutant using 82 monoclonal antibodies.
- Replication studies in canine and feline cell lines.
- Sequence analysis of the VP-1 and VP-2 genes of the mutant and wild-type CPV.
Main Results:
- A nonhemagglutinating CPV mutant was successfully generated.
- The mutant CPV remained antigenically indistinguishable from wild-type strains and replicated in relevant cell lines.
- Sequence analysis identified two nucleotide and two amino acid differences in the VP-1 and VP-2 genes at specific genome map units in the mutant.
- These mutations are hypothesized to be responsible for the altered hemagglutination phenotype.
Conclusions:
- The nonhemagglutinating CPV mutant provides a valuable tool for studying viral hemagglutination.
- Specific mutations within the VP-1 and VP-2 genes are strongly implicated in determining the hemagglutination ability of CPV.
- Further research is warranted to confirm the precise role of these mutations and their functional consequences.