Pathogenesis of Aleutian mink disease parvovirus infection: effects of suppression of antibody response on viral mRNA levels and on development of acute disease

Alexandersen, Søren; Storgaard, Torben; Kamstrup, N.; Aasted, Bent; Porter, David D.

doi:10.1128/jvi.68.2.738-749.1994

Cited by 21 publications

(19 citation statements)

References 63 publications

(111 reference statements)

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“…For example, suppression of anti-ADV antibody production by infected mink kits can be induced by administering antibodies to mink IgM. This lengthens the period during which these animals are susceptible to acute disease (Alexandersen et al, 1994). Furthermore, the passive transfer of maternal antibody to kits infected after birth prevents the development of pneumonia and is in this regard protective (Alexandersen et al, 1989).…”

Section: Multiple Roles For Antibody In the Pathogenesis Of Infectionmentioning

confidence: 99%

Pathogenesis of Aleutian Mink Disease Parvovirus and Similarities to B19 Infection

Best¹,

Bloom²

2005

Journal of Veterinary Medicine, Series B

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Aleutian mink disease parvovirus (ADV) is an unusual member of the autonomous parvoviruses in both its replication and pathogenesis. Infection of newborn mink kits results in an acute disease typified by virus replication in type II pneumocytes in the lung. This replication is permissive and cytopathic, characterized by the production of high levels of viral replicative intermediates and infectious progeny. However, infection of adult Aleutian mink leads to a chronic form of the disease termed Aleutian disease (AD). In this case, virus replication occurs predominantly in lymph node macrophages and is restricted, with viral DNA replication, RNA transcription, protein expression and production of infectious progeny occurring at low levels. B19 is the only autonomous parvovirus known to infect humans. The primary site of virus replication in both children and adults is in erythrocyte precursors in the blood and bone marrow, although viral genomes have been detected in various other tissues. B19 infection often causes a self-limiting disease although persistent infection of B19 can occur in both immuno-compromised and -competent people. Perhaps the most striking similarity between infection with ADV or with B19 is the important role the humoral immune response to infection has in pathogenesis. It can be both protective and pathogenic. Due to of the central role of antibody in the disease caused by either virus, understanding the specific roles of antibody production in protection, antibody-mediated enhancement of infection, the establishment of persistent infection and immune-mediated pathology will provide insight into the pathogenesis of these infections. A second similarity between the two viruses is the ability to establish persistent infection. Persistence of ADV is associated with restricted replication. Although many cellular factors may contribute to restricted virus replication, the interactions between the major non-structural protein, NS1, and the cells are likely to be critical. Parallels exist between the expression and post-translational modification of ADV and B19 NS1 proteins that may contribute to restriction of virus replication. Thus, a study of the regulation of NS1 expression and its interactions with cell signalling pathways may lead to increased understanding of the restricted replication of these two viruses, and perhaps of persistent infection.

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Section: Multiple Roles For Antibody In the Pathogenesis Of Infectionmentioning

confidence: 99%

Pathogenesis of Aleutian Mink Disease Parvovirus and Similarities to B19 Infection

Best¹,

Bloom²

2005

Journal of Veterinary Medicine, Series B

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“…Mink kits from seropositive dams or mink kits passively given anti-ADV antibodies do not develop acute disease but instead progress to develop the persistent form of the disease (3,7). Somehow, anti-ADV antibodies down regulate the viral DNA replication and transcription in infected cells in these mink kits (7,8).…”

mentioning

confidence: 99%

“…The replication of the cell culture-adapted strain of ADV is significantly slower than that of MEV in CRFK cells (14,55). When considered with the in vivo observations, it has led us to propose that low-level replication is an intrinsic property of ADV (8,55). Because of its potential involvement in the unique pathogenesis of ADV, we have been interested in exploring the molecular mechanisms governing this low-level replication.…”

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Two parvoviruses that cause different diseases in mink have different transcription patterns: transcription analysis of mink enteritis virus and Aleutian mink disease parvovirus in the same cell line

Storgaard

Oleksiewicz

Bloom

et al. 1997

J Virol

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The two parvoviruses of mink cause very different diseases. Mink enteritis virus (MEV) is associated with rapid, high-level viral replication and acute disease. In contrast, infection with Aleutian mink disease parvovirus (ADV) is associated with persistent, low-level viral replication and chronic severe immune dysregulation.In the present report, we have compared viral transcription in synchronized CRFK cells infected with either MEV or ADV using a nonradioactive RNase protection assay. The overall level of viral transcription was 20-fold higher in MEV-than in ADV-infected cells. Furthermore, MEV mRNA encoding structural proteins (MEV mRNA R3) was dominant throughout the infectious cycle, comprising approximately 80% of the total viral transcription products. In marked contrast, in ADV-infected cells, transcripts encoding nonstructural proteins (ADV mRNA R1 and R2) comprised more than 84% of the total transcripts at all times after infection, whereas ADV mRNA R3 comprised less than 16%. Thus, the ADV mRNA coding for structural proteins (ADV mRNA R3) was present at a level at least 100-fold lower than the corresponding MEV mRNA R3. These findings paralleled previous biochemical studies analyzing in vitro activities of the ADV and MEV promoters (J. Christensen, T. Storgaard, B. Viuff, B. Aasted, and S. Alexandersen, J. Virol. 67:1877-1886, 1993). The overall low levels of ADV mRNA and the paucity of the mRNA coding for ADV structural proteins may reflect an adaptation of the virus for low-level restricted infection. Downloaded from 4992 STORGAARD ET AL. J. VIROL. on July 7, 2020 by guest http://jvi.asm.org/ Downloaded from FIG. 4. Quantitative comparison of MEV and ADV transcription. Synchronized CRFK cells infected with either ADV or MEV were lysed at the indicated times after release from HU. The total amount of viral transcripts initiated from the different viral promoters was quantified by RPA and plotted on an arbitrary scale as a function of time after HU release. Transcripts initiated from the MEV P4 and ADV P3 promoters encode the nonstructural proteins, while transcripts initiated from the MEV P38 and ADV P36 promoters encode the structural proteins.

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“…A close correlation exists between the pathogenesis of disease induced by the Aleutian mink disease parvovirus (ADV) and viral replication at the single-cell level. Acute ADV infection of type II pneumocytes in mink kits is permissive and leads to a fulminant pneumonia (3,4,9,27). Chronic infection of adult mink, on the other hand, is associated with profound immune disturbances and restricted viral replication in lymphoid tissues (2,4,9,(20)(21)(22).…”

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Subcellular localization of Aleutian mink disease parvovirus proteins and DNA during permissive infection of Crandell feline kidney cells

Oleksiewicz¹,

Costello²,

Huhtanen³

et al. 1996

J Virol

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Confocal microscopy allowed us to localize viral nonstructural (NS) and capsid (VP) proteins and DNA simultaneously in cells permissively infected with Aleutian mink disease parvovirus (ADV). Early after infection, NS proteins colocalized with viral DNA to form intranuclear inclusions, whereas VP proteins formedhollow intranuclear shells around the inclusions. Later, nuclei had irregular outlines and were virtually free of ADV products. In these cells, inclusions of viral DNA with or without associated NS protein were embedded in cytoplasmic VP protein. These findings implied that ADV replication within an infected cell is regulated spatially as well as temporally.

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Pathogenesis of Aleutian mink disease parvovirus infection: effects of suppression of antibody response on viral mRNA levels and on development of acute disease

Cited by 21 publications

References 63 publications

Pathogenesis of Aleutian Mink Disease Parvovirus and Similarities to B19 Infection

Pathogenesis of Aleutian Mink Disease Parvovirus and Similarities to B19 Infection

Two parvoviruses that cause different diseases in mink have different transcription patterns: transcription analysis of mink enteritis virus and Aleutian mink disease parvovirus in the same cell line

Subcellular localization of Aleutian mink disease parvovirus proteins and DNA during permissive infection of Crandell feline kidney cells

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