The neurobiology of canine distemper virus infection

Vandevelde, M.; Zurbriggen, Andreas

doi:10.1016/0378-1135(95)00021-2

Cited by 72 publications

(42 citation statements)

References 46 publications

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“…The major sites of viral propagation are lymphoid tissues, and acute diseases are usually accompanied by profound lymphopenia and immunosuppression, leading to secondary and opportunistic infections (1,15,24,28). While CDV and phocine distemper virus often invade the central nervous systems of their hosts (46), encephalitis is not common in MV and RPV infections.…”

mentioning

confidence: 99%

Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

Tatsuo

Ono

Yanagi

2001

J Virol

305

283

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mentioning

confidence: 99%

Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

Tatsuo

Ono

Yanagi

2001

J Virol

305

283

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“…The degree and extent of the distemper-induced encephalomyelitis varies somewhat between the various strains of virulent virus. 2,3,5,12,13,15 A large number of dogs that were participating in a sled race in Kotzbue, Alaska, became ill with symptoms that were clinically consistent with canine distemper. Catarrh, mucopurulent nasal discharge, and neurological signs were noted in the affected animals.…”

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confidence: 99%

A Canine Distemper Outbreak in Alaska: Diagnosis and Strain Characterization Using Sequence Analysis

Maes

Wise

Fitzgerald³

et al. 2003

J VET Diagn Invest

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Abstract. Vaccination with modified-live vaccines has been very effective in reducing the incidence of canine distemper, a disease that can be devastating in unvaccinated populations. A diagnostic submission to the Animal Health Diagnostic Laboratory at Michigan State University, East Lansing, Michigan, involved a case in which several hundred dogs in an Alaskan town died in a suspected canine distemper outbreak. Cytoplasmic and intranuclear eosinophilic inclusion bodies, consistent with canine distemper virus (CDV) infection, were found in urinary bladder, spleen, lung, and salivary gland. Direct fluorescent antibody test gave results that could be considered positive for canine distemper. Because of the condition of the tissues received, the histopathology and fluorescent antibody-staining results were suggestive but not conclusive of CDV. In this study, immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and DNA sequencing were used to confirm the presence of canine distemper virus in these tissues and to perform molecular characterization of the virus. Immunohistochemistry showed the presence of the virus in spleen, lung, and salivary gland. Viral RNA was detected by RT-PCR in brain, spleen, liver, lung, and kidney, both with nucleoprotein and phosphoprotein (P)-gene-specific primers. Sequence alignment and phylogenetic analysis of a 540-bp P-gene fragment of the Alaskan strain with corresponding sequences of 2 vaccine and 7 wild-type CDV strains showed that the virus responsible for the outbreak was closely related to a virulent strain of distemper virus from Siberia.Canine distemper virus (CDV) is an enveloped negative-strand RNA virus classified under the genus Morbillivirus within the family of Paramxyoviridae. Canine distemper has a very broad host range, which includes Canidae, Mustelidea, Procyonidae, Ursidae, Viverridae, and Felidae. The clinical picture of CDV infection in dogs is considered to be dependent on virus strain characteristics, age and immune status of the affected animal, and environmental factors. When population immunity is high, many CDV infections are either clinically unapparent or result in a clinical picture that is relatively mild and may go unrecognized as distemper. When infection occurs in highly susceptible young animals, however, severe multisystemic disease can result. The time of onset of the immune response and, likely, also the virulence of the virus are critical factors in the extent of viral invasion of epithelial tissues and of the central nervous system. The degree and extent of the distemper-induced encephalomyelitis varies somewhat between the various strains of virulent virus. 2,3,5,12,13,15 A large number of dogs that were participating in a sled race in Kotzbue, Alaska, became ill with symptoms that were clinically consistent with canine distemper. Catarrh, mucopurulent nasal discharge, and neurological signs were noted in the affected animals. During the first week of this outbreak, approximately 200 Alaskan Huskies and other mixed-...

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“…The mortality rates following CDV infection vary with the host species, ranging from 0% in domestic cats to approximately 50% in domestic dogs and 100% in ferrets. Encephalomyelitis is the most common cause of death of CDV-infected animals (2,40,43). In dogs, CDV infection results in a progressive demyelinating encephalomyelitis, probably due to a bystander mechanism in which macrophages play an important role (46).…”

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confidence: 99%

Antibodies to CD9, a Tetraspan Transmembrane Protein, Inhibit Canine Distemper Virus-Induced Cell-Cell Fusion but Not Virus-Cell Fusion

Schmid¹,

Zurbriggen²,

Gassen

et al. 2000

J Virol

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Canine distemper virus (CDV) causes a life-threatening disease in several carnivores including domestic dogs. Recently, we identified a molecule, CD9, a member of the tetraspan transmembrane protein family, which facilitates, and antibodies to which inhibit, the infection of tissue culture cells with CDV (strain Onderstepoort). Here we describe that an anti-CD9 monoclonal antibody (MAb K41) did not interfere with binding of CDV to cells and uptake of virus. In addition, in single-step growth experiments, MAb K41 did not induce differences in the levels of viral mRNA and proteins. However, the virus release of syncytium-forming strains of CDV, the virus-induced cell-cell fusion in lytically infected cultures, and the cell-cell fusion of uninfected with persistently CDV-infected HeLa cells were strongly inhibited by MAb K41. These data indicate that anti-CD9 antibodies selectively block virus-induced cell-cell fusion, whereas virus-cell fusion is not affected.Canine distemper virus (CDV) causes in carnivores (canines, felids, ferrets, raccoons, and seals) a highly contagious disease with many similarities to human measles but also with a significant difference, as it is much more neurotropic and causes acute encephalitis in about half of the infected animals (2, 22). The disease is characterized by fever, coryza, conjunctivitis, gastroenteritis, and pneumonitis. The mortality rates following CDV infection vary with the host species, ranging from 0% in domestic cats to approximately 50% in domestic dogs and 100% in ferrets. Encephalomyelitis is the most common cause of death of CDV-infected animals (2, 40, 43). In dogs, CDV infection results in a progressive demyelinating encephalomyelitis, probably due to a bystander mechanism in which macrophages play an important role (46). The onset of encephalitis appears to be influenced by humoral immune responses to CDV (33). Canine distemper is also associated with transient immunosuppression that may result in significant morbidity and mortality through opportunistic infections (6,19).The cellular receptor for CDV is not known. It has been shown by complementation analysis with the help of recombinant envelope proteins of CDV and measles virus MV that the CDV H protein is responsible for the selective tropism of CDV in cell culture (39). Human-mouse somatic cell hybrids were used to demonstrate that human chromosome 19 encodes a CDV receptor on human cells (39). Recently, we obtained a monoclonal antibody (MAb K41) which was able to inhibit CDV infection and found that it recognizes the tetraspan transmembrane (TM4) protein CD9 (21), the gene of which is localized on human chromosome 12 (4, 5). However, direct binding of CDV to CD9 could not be demonstrated, suggesting that CD9 is not a receptor for CDV.CD9 has also been discussed as a possible cellular receptor for feline immunodeficiency virus (FIV) (44), and a different member of the TM4 superfamily, C33 (CD82), was found to be involved in syncytium formation by human T-cell leukemia virus type 1 (HTLV-1) (14). Similar...

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The neurobiology of canine distemper virus infection

Cited by 72 publications

References 46 publications

Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

A Canine Distemper Outbreak in Alaska: Diagnosis and Strain Characterization Using Sequence Analysis

Antibodies to CD9, a Tetraspan Transmembrane Protein, Inhibit Canine Distemper Virus-Induced Cell-Cell Fusion but Not Virus-Cell Fusion

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