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PubMed2000

Absence of measles virus and canine distemper virus transcripts in long-term bone marrow cultures from patients with Paget's disease of bone.

The presence of intranuclear inclusions in pagetic osteoclasts with similar characteristics to those seen in some slow viral diseases has lead to the hypothesis that Paget's disease is caused by a similar infection. Bone marrow aspirates from seven patients with hemipelvic Paget's disease were taken from both sides of the pelvis and cultured under identical conditions. RNA was extracted after approximately 2 weeks of culture and reverse transcriptase-linked polymerase chain reaction used to investigate the expression of measles and canine distemper virus RNA. We were unable to detect the presence of measles virus (MV) or canine distemper virus (CDV) transcripts in bone marrow cultures from either affected or unaffected sites in any of our patients. The results of this study do not support a role for MV or CDV in the pathogenesis of Paget's disease of bone.

Animals↗
PubMed1984

Measles virus and inactivated canine distemper virus induce incomplete immunity to canine distemper.

Pairs of specific pathogen free dogs were immunized with two injections of heat inactivated canine distemper virus (CDV) or one injection of a live CDV or live measles virus (MV) vaccine. Three unimmunized dogs were used as controls. All 9 dogs were challenged with virulent CDV (Snyder Hill strain). The three unimmunized dogs developed severe signs of disease with a lethal infection in one. The two dogs immunized with live CDV vaccine developed a strong humoral as well as cellular immune response after immunization and were protected against virus replication. Animals immunized with either inactivated CDV or modified live MV failed to develop a measurable cellular immune response after immunization and had a comparatively weak humoral immune response to distemper antigens. They showed mild signs of infection after challenge and responded with strong anamnestic cellular and humoral immunity. The measles vaccine immunized dogs had a moderate serum titer of measles hemolysin-inhibiting antibodies which, after exposure to distemper virus, was boosted to high levels. It is proposed that this response plays a role in the mitigation of the virulent distemper infection in these animals.

Animals↗
PubMed1995

The neurobiology of canine distemper virus infection.

Canine distemper virus (CDV) invades the nervous system and replicates in neurons and glial cell of the white matter during a period of severe viral induced immunosuppression. Demyelination occurs in infected white matter areas in the absence of inflammation. The mechanism of demyelination is not apparent because there is no ultrastructural evidence of viral replication in the oligodendrocytes, the myelin producing cells. However, brain tissue culture studies have shown that oligodendrocytes support transcription of all CDV genes and later on degenerate, although no viral proteins can be found in these cells. It remains to be shown how such a restricted infection leads to demyelination. Concomitant with immunologic recovery during the further course of the disease, inflammation occurs in the demyelinating lesions with progression of the lesions in some animals. A series of experiments in vitro suggested that chronic demyelination is due to a bystander mechanism associated with the virus-induced immune response in which antibody dependent cell-mediated reactions play an important role. The progressive, or even relapsing, course of the disease is associated with viral persistence in the nervous system. Persistence of CDV in the brain appears to be due to non-cytolytic selective spread of the virus with very limited budding. In this way CDV escaped immune surveillance.

Acute Disease↗
PubMed1994

Aspects of canine distemper virus and measles virus encephalomyelitis.

Canine distemper (CD) is a frequently fatal, systemic morbillivirus infection in the dog and other carnivores: encephalomyelitis is the common cause of death. Susceptibility to canine distemper virus (CDV) is now recognized in a wide range of non-domestic animals, most recently in captive lions, tigers and leopards. Furthermore, closely related viruses have produced CD-like diseases in marine mammals. CDV induces an inclusion-body encephalomyelitis in the dog and demyelination is often a conspicuous feature. Myelin injury is associated with the presence of virus but the mechanism of demyelination remains incompletely understood. Oligodendrocyte infection may be defective, as has been shown in vitro. CDV and measles virus (MV) produce similar systemic disorders in their respective hosts but differ markedly in the frequency of central nervous system (CNS) involvement, and in the pathogenesis of the more common neurological sequelae. Both CDV and MV have been considered as multiple sclerosis agents, and the association of CDV with other human disease has been suggested.

Animals↗
PubMed2006

Comparative trial of the canine parvovirus, canine distemper virus and canine adenovirus type 2 fractions of two commercially available modified live vaccines.

The results of vaccinating two groups of puppies with commercial vaccines, both of which claimed to provide adequate protection with a final vaccination at 10 weeks of age, were compared. Groups of 19 and 20 puppies with similar titres of maternally derived antibodies against canine parvovirus (cpv), canine distemper virus (cdv) and canine adenovirus type 2 (cav-2) at four weeks of age were vaccinated at six and 10 weeks of age and their responses to each vaccination were measured by comparing the titres against cpv, cdv and cav-2 in the serum samples taken immediately before the vaccination and four weeks later. After the vaccination at six weeks of age, all 19 of the puppies in group 1 had responded to cpv and cdv, and 14 had responded to cav-2; in group 2, 17 of the 20 had responded to cpv, 19 to cdv and 15 to cav-2. In both groups the puppies that did not respond to the first vaccination had responded serologically to cpv, cdv and cav-2 at 10 weeks of age.

Adenoviridae Infections↗
PubMed1997

Antibody responses of red wolves to canine distemper virus and canine parvovirus vaccination.

Twenty captive red wolves (Canis rufus), including 16 intended for release into Great Smoky Mountains National Park, Cades Cove, Tennessee (USA), and four housed at Knoxville Zoological Gardens, Inc., Knoxville, Tennessee, were evaluated for immunologic response to vaccination between June 1994 and April 1995. Wolves were vaccinated with modified-live (MLV) canine distemper virus (CDV) and canine parvovirus type-2 (CPV2). Sera were collected, and immunofluorescent staining was performed for determination of immunoglobulin titers (CDV IgM, CDV IgG, and CPV2 IgG). A capture enzyme-linked immunosorbent assay was performed for validation purposes, to confirm the reactivity of our standard diagnostic reagents with red wolf serum. All wolves produced a measurable antibody response to CDV and CPV2 vaccination. Titers against CDV and CPV2 varied widely among individual wolves, but between-litter differences in mean titers were not significant. No consistent response between the degree of response to CDV versus CPV2 vaccination was observed in individual wolves. No differences were seen between IgG responses of pups vaccinated with univalent vaccines given concurrently or during alternating weeks. Pups had an IgG response to CDV and CPV2 vaccination as early as 9 wk of age. Mean post-vaccination IgG titers against CDV were at or above the level normally measured in vaccinated domestic dogs. Mean post-vaccination IgG titers against CPV2 were below the level normally measured in domestic dogs. Adult previously-vaccinated wolves had measurable CDV and CPV2 IgG titers more than 1 yr after vaccination, but did not have significant IgG titer increases after revaccination. We conclude that red wolves are capable of producing an antibody response after vaccination with commercial canine products but that their response to CPV2 vaccination was minimal. This response can be assayed using tests developed for domestic dogs.

Aging↗
PubMed2006

Adaptation of canine distemper virus to canine footpad keratinocytes modifies polymerase activity and fusogenicity through amino acid substitutions in the P/V/C and H proteins.

The wild-type canine distemper virus (CDV) strain A75/17 induces a non-cytocidal infection in cultures of canine footpad keratinocytes (CFKs) but produces very little progeny virus. After only three passages in CFKs, the virus produced 100-fold more progeny and induced a limited cytopathic effect. Sequence analysis of the CFK-adapted virus revealed only three amino acid differences, of which one was located in each the P/V/C, M and H proteins. In order to assess which amino acid changes were responsible for the increase of infectious virus production and altered phenotype of infection, we generated a series of recombinant viruses. Their analysis showed that the altered P/V/C proteins were responsible for the higher levels of virus progeny formation and that the amino acid change in the cytoplasmic tail of the H protein was the major determinant of cytopathogenicity.

Adaptation, Biological↗
PubMed2003

Mechanism of reduction of virus release and cell-cell fusion in persistent canine distemper virus infection.

Canine distemper virus (CDV), a mobillivirus related to measles virus causes a chronic progressive demyelinating disease, associated with persistence of the virus in the central nervous system (CNS). CNS persistence of morbilliviruses has been associated with cell-to-cell spread, thereby limiting immune detection. The mechanism of cell-to-cell spread remains uncertain. In the present study we studied viral spread comparing a cytolytic (non-persistent) and a persistent CDV strain in cell cultures. Cytolytic CDV spread in a compact concentric manner with extensive cell fusion and destruction of the monolayer. Persistent CDV exhibited a heterogeneous cell-to-cell pattern of spread without cell fusion and 100-fold reduction of infectious viral titers in supernatants as compared to the cytolytic strain. Ultrastructurally, low infectious titers correlated with limited budding of persistent CDV as compared to the cytolytic strain, which shed large numbers of viral particles. The pattern of heterogeneous cell-to-cell viral spread can be explained by low production of infectious viral particles in only few areas of the cell membrane. In this way persistent CDV only spreads to a small proportion of the cells surrounding an infected one. Our studies suggest that both cell-to-cell spread and limited production of infectious virus are related to reduced expression of fusogenic complexes in the cell membrane. Such complexes consist of a synergistic configuration of the attachment (H) and fusion (F) proteins on the cell surface. F und H proteins exhibited a marked degree of colocalization in cytolytic CDV infection but not in persistent CDV as seen by confocal laser microscopy. In addition, analysis of CDV F protein expression using vaccinia constructs of both strains revealed an additional large fraction of uncleaved fusion protein in the persistent strain. This suggests that the paucity of active fusion complexes is due to restricted intracellular processing of the viral fusion protein.

Animals↗
PubMed1993

Fusion protein gene nucleotide sequence similarities, shared antigenic sites and phylogenetic analysis suggest that phocid distemper virus type 2 and canine distemper virus belong to the same virus entity.

Nucleotide sequencing of the fusion protein (F) gene of phocid distemper virus-2 (PDV-2), recently isolated from Baikal seals (Phoca sibirica), revealed an open reading frame (nucleotides 84 to 2075) with two potential in-frame ATG translation initiation codons. We suggest that the second in-frame ATG triplet at positions 264 to 266 initiates the translation, resulting in a protein of 537 amino acid residues with a calculated M(r) of 63,035. The putative F1/F2 cleavage site, located approximately 100 amino acid residues from the N terminus, is identical to those of the F proteins of phocid distemper virus-1 (PDV-1) isolated from European harbour seals (Phoca vitulina) and of canine distemper virus (CDV). A full scale comparison of morbillivirus F genes reveals that the conserved F0 extracellular protein-encoding region contains a large number of non-expressed mutations, suggesting that this part of the protein is under strong functional constraints. Phylogenetic analysis of morbillivirus F gene nucleotide sequences revealed a closer evolutionary relationship between PDV-2 and CDV than between PDV-1 and PDV-2. These data were supported by cross-reactivity patterns of PDV-2 and CDV obtained with monoclonal antibodies to structural proteins of PDV-1 and CDV, and suggest that PDV-2 is a strain of CDV, resulting from a trans-species infection.

Amino Acid Sequence↗
PubMed1970

Continuous-flow ultracentrifugation of canine distemper virus and infectious canine hepatitis virus.

The use of a Spinco L-4 zonal centrifuge with the B-XVI continuous-flow rotor for the purification of canine distemper and infectious canine hepatitis viruses is described. Up to 68 liters of virus was processed at one time. Infectious canine hepatitis virus was found to band at 39% sucrose and canine distemper virus banded between 32 and 48% sucrose. The virus was concentrated 10-fold, and the purity of the virus, as measured by protein concentration, was increased by 99%.

Adenoviruses, Canine↗
PubMed1991

Detection of phocid distemper virus RNA in seal tissues using slot hybridization and the polymerase chain reaction amplification assay: genetic evidence that the virus is distinct from canine distemper virus.

Slot hybridization and the polymerase chain reaction (PCR) after reverse transcription (RT) were used to detect RNA extracted from tissues of seals after naturally occurring disease and experimental infection with phocid distemper virus (PDV). A phosphoprotein (P) gene-specific cDNA served as a probe for both slot hybridization and the identification of PCR-generated fragments by Southern blotting. As primers for the PCR assay PDV P gene-derived oligonucleotides were used. Hybridization, PCR and partial nucleic acid sequence analysis clearly demonstrated that PDV is a distinct virus (most closely related to canine distemper virus) within the morbillivirus group. PCR, when combined with Southern blot hybridization, was clearly superior to slot hybridization and more sensitive than cell culture isolation and immunofluorescence assays for the detection of virus in tissues. Considerable amounts of viral RNA could be demonstrated in the lungs and spleens. In experimentally infected animals a large quantity of virus-specific RNA was additionally found in colon samples. Using RT-PCR in combination with Southern blotting. PDV could be demonstrated in buffy coat cells using a simple and fast cell lysis procedure.

Animals↗
PubMed1995

Canine distemper virus persistence in the nervous system is associated with noncytolytic selective virus spread.

Canine distemper virus (CDV), a negative-strand RNA morbillivirus, causes a progressive demyelinating disease in which virus persistence plays an essential role. The antiviral immune response leads to virus clearance in the inflammatory lesions. However, CDV can replicate and persist outside these inflammatory lesions within the brain. How CDV is capable of persisting in the presence of an effective antiviral immune response is poorly understood. In the present investigation, we studied several aspects of virus replication in primary dog brain cell cultures (DBCC), comparing an attenuated CDV strain and a virulent CDV strain. Confluent DBCC were infected with either virulent A75/17-CDV or attenuated Onderstepoort-CDV and monitored for 60 days. Persistence was not associated with defective virus production, because all mRNAs and corresponding proteins were continuously expressed in the noncytolytic infection. Quantitative measurements did not detect a difference between the two types of infection in the rate of virus transcription and protein synthesis at the level of the single cell. However, electron microscopy and virus titration experiments showed that in the persistent CDV infection virus budding is strongly limited compared with that of the attenuated virus. Morphometry and immunocytochemistry showed profound differences in the way the two viruses spread in the culture. The attenuated CDV spread randomly to immediately adjacent cells, whereas persistent CDV spread selectively to more-distant cells by way of cell processes. In conclusion, the present study supports a mechanism of CDV persistence through selective spread by way of cell processes, enabling virulent CDV to invade the central nervous system without the need of releasing much virus into the extracellular space.

Animals↗