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At least 487 records · Page 27Linked to original sources
PubMed1989

Chronic relapsing demyelinating encephalomyelitis associated with persistent spontaneous canine distemper virus infection.

This is the first report of spontaneous canine distemper virus (CDV) infection in a dog associated with chronic progressive multiphasic neurological disease. Initial neurological deficits in the pelvic limbs progressed rapidly to paraplegia with almost complete remission after 9 weeks. Then another acute episode occurred with severe thoracic limb deficits and cerebellar dysfunction and progressive neurological deterioration over 3 months with rising serum neutralizing (SN) anti-CDV titers in the serum and cerebrospinal fluid (CSF). Three neuropathologically distinct lesions of spinal cystic necrosis, chronic demyelinating foci in the cerebellum and acute demyelinating encephalitis in the pons were identified. Persistent CDV antigen was demonstrated immunocytochemically only in acute lesions and atypically restricted to neurons. However, the immunological mechanism associated with the distinct remissions and exacerbations and CDV antigen clearance from chronic demyelinating lesions but persistence in acute lesions, despite a vigorous anti-CDV serologic response, was not defined.

Animals↗
PubMed1983

Glial proteins in canine distemper virus-induced demyelination. A sequential immunocytochemical study.

A temporal series of demyelinating lesions in experimental canine distemper virus (CDV) infection was examined with immunohistological techniques demonstrating myelin basic protein (MBP), myelin-associated glycoprotein (MAG), and glial fibrillary acidic protein (GFAP) on serial sections. The earliest lesions were characterized by decreased MBP and MAG and increased GFAP. During the further progression of the disease, MBP and MAG losses continued to match each other. There was no indication of MAG loss preceding the disappearance of MBP. In the more advanced lesions there was a marked decrease of GFAP positive cells. Since these findings differed considerably from similar immunohistochemical studies in progressive multifocal leukoencephalopathy (PML) where demyelination results from oligodendroglial infection, it was concluded that the oligodendroglial cell body is not the primary target of CDV. The marked astroglial changes were also considered to contribute to demyelination in CDV infection but the mechanism by which this happens remains unknown.

Animals↗
PubMed1978

Canine distemper virus-associated encephalitis: modification by passive antibody administration.

Gnotobiotic puppies were intraperitoneally infected with R252-canine distemper virus (CDV), and treated with normal serum (NS) or CDV-specific antibody. Resultant central nervous system (CNS) lesions were evaluated by light and immunofluorescence microscopy. Lesions in NS-treated dogs, if present, consisted of small foci of neuronal degeneration and accompanying microgliosis, restricted to grey matter of the frontal lobe. Dogs receiving anti-CDV antibody, in contrast, had extensive lesions in the brain. Laminar cortical necrosis, gliosis and astrocytic activation of the grey matter of the frontal lobe was the most consistent lesion observed. In addition, foci of cerebellar granule cell layer degeneration and necrosis was seen along with segmental poliomalacia of the spinal cord. In several dogs, eosinophilic intracytoplasmic and intranuclear viral inclusion bodies were observe in neurons. The lesions observed in these dogs are compared to previously reported lesions of CDV infection in dogs.

Animals↗
PubMed1993

In vivo and in vitro expression of canine distemper viral proteins in dogs and non-domestic carnivores.

The occurrence of the nucleo-, phospho-, matrix, fusion, and hemagglutinin proteins of the canine distemper virus (CDV) was investigated immunocytochemically in the brains of 3 dogs, 6 stone martens, 1 polecat, and 1 weasel. In addition, viral protein expression was studied in primary brain cell cultures of the 3 dogs after co-cultivation with Vero cells. Immunohistochemically, only minor differences, restricted to the H-4 epitope, were noted between the various species and CDV isolates. The data presented indicate that the mustelid virus is antigenically not distinct from the canine morbillivirus.

Animals↗
PubMed1980

Persistent in vitro interaction of virulent and attenuated canine distemper virus with bovine cells.

Bovine macrophage and non-macrophage cultures were infected with either virulent or attenuated canine distemper virus (CDV). Macrophages were resistant to virulent CDV; however, they supported growth of the attenuated virus. Non-macrophage cultures supported growth of both virus variants in a persistent, non-lytic manner. Major differences between these two systems of in vitro viral persistence were seen in the host cell spectrum of progeny virus and the outcome of cocultivation experiments with Vero cells. Results obtained indicate that in vivo virulence of CDV is not linked to maturation in a macrophage, but rather, propagation in a given cell culture system results in selective growth of virulent or attenuated viral mutants. It is further concluded that in vivo virulence and in vitro growth potential of CDV are disparate properties of the virion.

Animals↗
PubMed1999

Early T cell response in the central nervous system in canine distemper virus infection.

The initial demyelinating lesions in canine distemper virus (CDV) infection develop during a period of severe immunosuppression in the absence of inflammation. In vitro and in vivo studies suggest that early demyelination is due to directly virus-induced oligodendroglial changes. In the present spatiotemporal study in experimentally CDV-infected dogs we observed diffuse up-regulation of T cells throughout the central nervous system (CNS) and T cell invasion in early demyelinating lesions. Invasion of T cells in the CNS occurred despite severe immunosuppression and without any perivascular cuffing. However, the major fraction of invading T cells correlated with sites of viral replication and coincided with the demonstration of an early immune response against the nucleocapsid protein of CDV. Activation of microglial cells was thought to have elicited the migration of T cells to the CNS by secretion of chemokines: marked IL-8 activity was found in the CSF of dogs with acute lesions. In areas of early demyelination, large numbers of CD3+ cells accumulated in the tissue in the absence of any morphological sign of inflammation. Whether the T cells at lesion sites contribute to the development of acute demyelination remains uncertain at this stage. Antiviral cytotoxicity was not apparent since viral clearance in demyelinating lesions is only effective when B cells and concurring antiviral antibody production appeared in the subacute and chronic inflammatory stage of the disease. CD3+ cells appear to persist for several weeks after infection since they were also found in recovered dogs that did not develop demyelination. Accumulation of immune cells, including a significant proportion of resting T cells (CD45RA+) in the CNS in the early stages of the disease may facilitate the later development of the intrathecal immune response and associated immunopathological complications.

Animals↗
PubMed2004

An mRNA region of the canine distemper virus fusion protein gene lacking AUG codons can promote protein expression.

Canine distemper virus (CDV) produces a glycosylated type I fusion protein (F) with an internal hydrophobic signal sequence beginning around 115 residues downstream of the first AUG used for translation initiation. Cleavage of the signal sequence yields the F0 molecule, which is cleaved into the F1 and F2 subunits. Surprisingly, when all in-frame AUGs located in the first third of the F gene were mutated a protein of the same molecular size as the F0 molecule was still expressed from both the Onderstepoort (OP) and A75/17-CDV F genes. We designated this protein, which is initiated from a non-AUG codon protein Fx. Site-directed mutagenesis allowed to identify codon 85, a GCC codon coding for alanine, as the most likely position from which translation initiation of Fx occurs in OP-CDV. Deletion analysis demonstrated that at least 60 nucleotides upstream of the GCC codon are required for efficient Fx translation. This sequence is GC-rich, suggesting extensive folding. Secondary structure may therefore be important for translation initiation at codon 85.

Amino Acid Substitution↗
PubMed1984

Canine distemper and experimental allergic encephalomyelitis in the dog: comparative patterns of demyelination.

The pattern of virus-induced and allergic demyelinating encephalomyelitis in the dog were compared. The predominant pattern of myelin loss in canine distemper (CD) infection was focal, periventricular and was initially noninflammatory. In contrast, sensitization to myelin produced a uniform pattern of central nervous system (CNS) myelinolysis which was disseminated, inflammatory and perivascular. Ultrastructurally, virus-infected neuroglia participated in the demyelination in CD, whereas infiltrating haematogenous mononuclear cells predominated in the lesions of experimental allergic encephalomyelitis (EAE). Areas of predilection within the CNS differed, being influenced by viral spread in CD and by vascular factors in EAE. In CD, the paramyxovirus appears to play a central role in the process of demyelination. In contrast to EAE, however, these studies do not support the view that autoreactivity to myelin contributes to the pathogenesis of CD demyelinating encephalomyelitis.

Animals↗
PubMed1985

Syncytia formation: an aid in the diagnosis of canine distemper encephalomyelitis.

Syncytia formation has been observed in response to experimental Canine Distemper Virus (CDV) infection in specific-pathogen-free Beagle dogs. Multinucleated giant cells are most frequently found in white matter lesions of the brain and in the anterior uvea of the eye. Lymph nodes and the lung are occasionally positive, while the leptomeninges will also rarely harbour syncytia. The mechanism of syncytia formation and their possible importance in the pathogenesis of the disease are briefly discussed. Widespread tissue syncytia formation is a feature of CDV infection which should assist in identifying cases of non-suppurative encephalitis in the dog caused by this agent.

Animals↗
PubMed1993

The use of monoclonal antibodies specific for seal immunoglobulins in an enzyme-linked immunosorbent assay to detect canine distemper virus-specific immunoglobulin in seal plasma samples.

A method is described for the measurement of antigen-specific immunoglobulin in seal pup plasmas. Four monoclonal antibodies (H1a, H13a, H24b and H49a) raised against grey seal (Halichoerus grypus) immunoglobulin were used in an ELISA procedure. Levels of canine distemper virus (CDV) specific macroglobulin (IgM like protein) were found to peak approximately 10 days after the first vaccination. Levels of other smaller CDV-specific immunoglobulins (IgG like protein) also increased after vaccination. Using immunoblotting the CDV specific IgG-like protein reacted with a CDV protein, having a molecular weight of approximately 75 kDa.

Animals↗
PubMed1976

On the development of CNS lesions in natural canine distemper encephalomyelitis.

Acute lesions within spinal cord white matter have been studied by light and electron microscopy in 3 dogs suffering from the acute form of canine distemper encephalomyelitis (CDE). Prominent features of these lesions were viral inclusions, giant cell formation, cellular degeneration, myelin breakdown and phagocytic activity by cells believed to be derived from local glia. The viral inclusions occurred in giant cells, many astrocytes, macrophages and occasional oligodendroglia. Only suggestions of active viral replication from cell membranes were present. On the basis of the above features, these CDE lesions were classed as being acute. Perivascular inflammation and parenchymal invasion by haematogenous cells were lacking. However, older, gliotic, demyelinated lesions were always associated with inflammation. The pattern of demyelination in acute CDE lesions differed from those seen in other conditions, in particular the autoimmune demyelinating diseases. In acute CDE lesions, individual fibres became separated from others by rings of cells, the processes of which systematically stripped the myelin from the outer layers of the sheath inwards until a naked segment of axon remained. Some of the macrophages were recognisable as astroglia. Elsewhere, unequivocal astrocytes containing myelin debris were common. The results suggest that inflammation in acute CDE lesions is not a primary event, and that viral invasion causes breakdown of tissue which is accompanied pari passu by myelin destruction. The latter might be related to the non-specific release of host factors (viz. hydrolytic enzymes) or humoral factors during the cellular degeneration. Local cells appeared to participate in the process of myelin phagocytosis. Overt inflammation and damage by haematogenous cells were features only of chronic lesions and have been described previously in studies on chronic CDE lesions. The results are interpreted in terms of their relevance to the study of human subacute sclerosing panencephalitis, of which CDE is considered the animal analogue, and multiple sclerosis, the paradigm of the human demyelinating diseases.

Animals↗
PubMed1979

Neutralizing antibodies to canine distemper and measles virus in multiple sclerosis.

Serum neutralizing antibody to canine distemper virus (CDV) was measured in 142 patients with multiple sclerosis (MS), an equal number of age and sex-matched normal controls, and 75 patients with other neurological disorders. An elevated antibody titer was found in the MS population compared to controls. Measles-neutralizing antibody was also found to be elevated in 128 patients with MS. The mean ratio of measles to CDV antibody was similar in the control and MS groups, but a wide range of measles to CDV ratios was found in individual patients and controls. No significant correlation was found between IgG levels and neutralizing antibody titers in MS sera. While the increased titer of measles and CDV antibody may represent a non-specific immunological response, these findings are also consistent with the hypothesis that CDV or a closely related measles virus may stimulate the increased level of measles and CDV antibodies found in MS sera.

Adolescent↗
PubMed1980

Pet ownership, distemper antibodies and multiple sclerosis.

The incidence of cat or dog ownership was similar in 64 multiple sclerosis (MS) patients in south-east England and age- and sex-matched controls. 86% of both groups had owned a cat or dog before the date of onset of MS in the index case so that it would be difficult to detect an association between pet ownership and MS. The titres of neutralising antibody to canine distemper virus were higher in the MS patients (mean 48 +/- 68) than the controls (32 +/- 35), a significant difference (P < 0.05). This difference is not necessarily explained by a cross-reaction with measles antibody of which the titre was much higher in MS (610 +/- 560) than in the controls (320 +/- 330, P < 0.001).

Animals↗
PubMedDate not supplied

Canine distemper virus infection of weanling mice. Pathogenesis of CNS disease.

Intracerebral inoculation of canine distemper virus (CDV) into weanling BALB/c, ICR an SJL mice produced acute encephalitis 2 - 3 weeks later. All animals that became ill exhibited lethargy an hind-limb paralysis followed by death. BALB/c mice were more susceptible to CDV than ICR or SJL mice. Pathologic changes were characterized primarily by meningitis and focal areas of parenchymal inflammation, necrosis and microglial hypertrophy. CDV was readily isolated from infected mouse brain 10 - 23 days after infection, and peak virus titers occurred at the height of neurologic disease 14 - 17 days after infection. CDV antigen was selected by immunofluorescence throughout grey and white matter of the brain and brain stem. CDV was rescued from explanted mouse brain tissue after it could not be isolated from brain homogenates. BALB/c mice which were inoculated intracerebrally with CDV one month after initial virus injection developed meningitis and a non-inflammatory degeneration of white matter.

Animals↗
PubMed1982

A study of measles virus and canine distemper virus antibodies, and of childhood infections in multiple sclerosis patients and controls.

We investigated the levels of neutralizing antibodies to measles virus and canine distemper virus (CDV) in 72 multiple sclerosis patients (MS) and matched controls and also examined the frequency and age of onset of a number of childhood illnesses, including measles. The frequency of each childhood illness was not significantly different between cases and controls, but cases did report a later age at measles infection. Our data suggest that the risk of MS is increased by a factor of 1.9 if measles infection occurs between 5 and 9 years of age. A validity survey, based on a questionnaire to general practitioners, suggested substantial inaccuracy in the patients' reports of when they had measles, but the direction and degree of inaccuracy did not appear to be different between cases and controls. We also found higher titres of neutralizing antibodies in cases than controls to both measles virus and CDV, although the CDV difference was not statistically significant. In the light of a significant correlation between measles and CDV titres in both cases and controls, we used paired logistic regression to determine if the case-control difference in titres for each virus could be explained by a confounding effect on one by the other. The numbers were too small, however, to enable us to separate out any independent association of either virus with MS.

Age Factors↗
PubMed1987

Demyelinating, non-demyelinating and attenuated canine distemper virus strains induce oligodendroglial cytolysis in vitro.

A virulent canine distemper virus (CDV) strain that causes demyelination in vivo has been shown to induce oligodendroglial degeneration in vitro. In order to investigate if this effect on oligodendrocytes is specific for demyelinating strains only, primary brain cell cultures were infected with either virulent demyelinating strains (A75/17 and CH84-CDV), a virulent non-demyelinating strain (SH-CDV) or a non-virulent strain (OP-CDV). All virulent viruses caused a persistent type infection with moderate cytolysis whereas the non-virulent strain was highly cytolytic. All strains induced a similar pattern of oligodendroglial degeneration. It was concluded that the ability to induce oligodendroglial degeneration, which is thought to be the in vitro correlate of demyelination in vivo, is inherent to CDV irrespective of the strain. The discrepancy between biological behaviour of CDV strains in brain cell cultures and in vivo can be explained by the more complex virus-cell interactions in vivo than in vitro.

Animals↗
PubMed1987

F1 polypeptides of two canine distemper virus strains: variation in the conserved N-terminal hydrophobic region.

The fusion protein of canine distemper virus was isolated by immunoadsorption from two virus strains, the rapidly growing Onderstepoort strain (forming large plaques) and the Convac vaccine strain (forming microplaques). The F1 subunits of the two fusion proteins were purified by preparative polyacrylamide gel electrophoresis. Direct amino acid sequence analysis revealed that 36-residue N-terminal regions of the proteins from the two strains are identical except at position 9, where Ala in the Convac strain is substituted by Val in the Onderstepoort strain. The two sequences show high homology with the previously determined N-terminal sequence of the F1 polypeptide of measles virus, and moderate homology with corresponding sequences of five paramyxoviruses, emphasizing the occurrence of an extensive conservation of these structures.

Amino Acid Sequence↗