Leland E. Carmichael

Evidence for evolution of canine parvovirus type 2 in Italy.

Two isolates of canine parvovirus (CPV) were obtained from dogs affected with severe haemorrhagic diarrhoea. Type 2b antigenic specificity was predicted by both antigenic analysis with monoclonal antibodies and PCR characterization with type-specific primers. Nevertheless, sequence analysis of the capsid protein-encoding gene revealed two amino acid changes. One of the changes affected position 426 (Asp to Glu), in a major antigenic site of the viral capsid, determining the replacement of a residue unique to CPV type 2b. The failure of established typing methods to distinguish this antigenic variant was overcome by the development of an RFLP assay.

Canine viral enteritis.

Canine viral enteritis should be suspected in dogs with an acute onset of vomiting and diarrhea, especially in puppies and where several animals are affected simultaneously. Definitive diagnosis requires laboratory confirmation, most often detection of viral particles in the stool. No diagnostic test is entirely specific or absolutely sensitive, however, and laboratory findings should be weighed accordingly. Immunization is the key to successful control. Effective vaccines for canine parvovirus are available. Maternal antibody suppresses response to vaccination in young pups and is the major problem in the control of infection. Vaccines against canine rotavirus and coronavirus are not available. The need for such vaccines and the feasibility of their effective use have not yet been clearly demonstrated.

Antigenic relationships between canine parvovirus type 2, feline panleukopenia virus and mink enteritis virus using conventional antisera and monoclonal antibodies.

SummaryThe antigenic relationships between three similar parvoviruses, canine parvovirus type 2 (CPV), feline panleukopenia virus (FPV) and mink enteritis virus (MEV) were investigated. Antisera against all 3 viruses and monoclonal antibodies (mAb) to CPV were prepared and the viruses compared using several serological methods. When conventional sera were used in the hemagglutination-inhibition and agar gel precipitin (AGP) tests there were no differences between the CPV viral isolates studied, but antigenic differences were revealed between the CPV isolates and the FPV or MEV. Of 16 mAb produced against CPV, six reacted only with the CPV. The other 10 mAb reacted with all three parvoviruses. Additionally, an antigenic difference was detected by AGP tests between one FPV isolate and the other FPV and MEV isolates. Including both conventional sera and mAb to CPV in a single AGP test with the CPV, MEV and FPV antigens permitted the comparison of results obtained with the different antibodies. The results reported revealed antigenic differences between CPV and FPV or MEV that were most clearly defined using mAb.

The global spread and replacement of canine parvovirus strains.

Canine parvovirus type 2 (CPV-2) became widespread during 1978 and was reported in many countries during 1978 and 1979. Earlier studies showed that CPV-2 was replaced in the U.S.A. around 1980 by an antigenically and genetically variant virus (CPV-2a). Here we show that CPV-2 was present in the U.S.A., Japan, Belgium and Australia prior to 1980, but that between 1979 and 1982 CPV-2 was replaced by CPV-2a in all of those countries as well as in France and Denmark. Examination of sera collected between 1979 and 1984 from wild coyotes (Canis latrans) in the U.S.A. by an agar gel precipitin assay indicated that the coyotes were originally infected by CPV-2, but that after 1980 the juvenile coyotes were being infected with CPV-2a. The natural global replacement of CPV-2 by CPV-2a over a period of 2 to 3 years indicates that CPV-2a has a strong epidemiological advantage over CPV-2, although the mechanism involved remains to be defined.

Detection and molecular characterization of a canine norovirus.

We identified a novel calicivirus in a pup with enteritis. The isolate was related genetically (90.1% aa identity in the capsid protein) to a lion norovirus strain.

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.

Canine host range and a specific epitope map along with variant sequences in the capsid protein gene of canine parvovirus and related feline, mink, and raccoon parvoviruses.

Canine parvovirus (CPV) is a recently recognized pathogen of dogs that is similar to the long-recognized feline, mink, and raccoon parvoviruses. Relationships between the viruses determined from DNA sequences of the capsid protein genes of 10 virus isolates showed the CPV isolates to be closely related to the other viruses, although comprising a distinct group. No immediate ancestor of CPV was observed amongst the mink, cat, or raccoon viruses examined. Three different directly repeated sequences were present within the noncoding region downstream from the capsid protein genes. Analysis of recombinants between CPV and feline panleukopenia virus at restriction sites within the capsid protein genes mapped a CPV-specific neutralization epitope on the virus capsid, differences in the pH dependence of hemagglutination, and part of the determinant of canine host range between 59 and 64 genome map units (m.u.). Those differences were therefore the result of up to three nucleotide or predicted amino acid sequence differences in that region. A second region between 64 and 73 m.u., which may affect the viability of certain recombinant viruses, contained four nucleotide differences, one of which was a coding change.

Specificity among barley yellow dwarf viruses in enzyme immunosorbent assays

Parallel homologous and heterologous enzyme-linked immunosorbent assays revealed a marked homologous specificity among four isolates of barley yellow dwarf virus (BYDV). Relatively weak heterologous reactions permitted division of the viruses into two groups. The RPV and RMV isolates have some common antigens, but appear to be unrelated to the MAV and PAV isolates, which are related to each other. A fifth BYDV isolate, SGV, did not react strongly with any of the four virus-specific globulins studied, but faint reactions suggested a relationship with PAV.

Characterization of BPV-like DNA in equine sarcoids.

SummaryThe DNA from equine sarcoid samples from New York State and Switzerland was isolated and probed with bovine papillomavirus type 1 (BPV-1) to determine if BPV genomes were present. Twelve of 13 sarcoids from New York State and 17/20 sarcoids from Switzerland contained DNA that hybridized to the BPV-1 probe. Restriction enzyme analysis of the positive samples demonstrated restriction fragment profiles characteristic of BPV-1 in 22 sarcoids and restriction fragment profiles characteristic of bovine papillomavirus type 2 (BPV-2) in 7 sarcoids. In addition, three tissues histologically diagnosed as pyogranulomatous dermatitis, fibropapilloma, and fibrosarcoma contained BPV-like DNA. Tissues with BPV-1-like and BPV-2-like DNA contained an average of 285.7 (21 to 808) and 125.8 (2 to 762) BPV-like genomes per cell, respectively. Minor differences in the restriction fragment profiles of the BPV-like DNA and evidence for partial BPV-like genomes were found in some sarcoids. BPV-like DNA was not detected in lymphocyte DNA from sarcoid-affected horses. These results confirm previous observations and support the hypothesis that bovine papillomavirus, or a very similar virus, is linked to the cause of equine sarcoid.

Minute Virus of Canines (MVC, Canine Parvovirus Type-1): Pathogenicity for Pups and Seroprevalence Estimate

Minute virus of canines (MVC, canine parvovirus type-1) caused inapparent to severe illness in neonatal specific-pathogen-free pups exposed by the oronasal route. The experimental disease was generally mild. Four of 21 infected pups had clinical signs of respiratory illness, but only 2 pups, not euthanized during the early postinoculation period, developed severe illness or died. Principal pathologic changes included bronchitis and interstitial pneumonia with various degrees of lymphadenitis. In contrast to the reported field cases, enteric signs were absent in the experimentally infected animals. Histopathologic changes in the small intestine were mild or absent. Bronchial, bronchiolar, and alveolar epithelial cells appeared to be the sites of initial and most extensive viral growth, reflecting the pattern of histopathologic changes. The disease caused by MVC was mild in comparison to that caused by canine parvovirus-type 2. MVC now appears to be established as a cause of illness in young pups and of transplacental infections with embryo resorption. The prevalence of MVC hemagglutination-inhibiting antibodies was high (~50%) in adult dog sera from widely separated geographic areas of the United States.