Aleutian Mink Disease - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Aleutian Mink Disease

The Experts below are selected from a list of 678 Experts worldwide ranked by ideXlab platform

Aleutian Mink Disease – Free Register to Access Experts & Abstracts

Marshall E. Bloom – One of the best experts on this subject based on the ideXlab platform.

James B. Wolfinbarger – One of the best experts on this subject based on the ideXlab platform.

  • Caspase Cleavage of the Nonstructural Protein NS1 Mediates Replication of Aleutian Mink Disease Parvovirus
    Journal of virology, 2003
    Co-Authors: Sonja M. Best, James B. Wolfinbarger, Janie F. Shelton, Justine M. Pompey, Marshall E. Bloom
    Abstract:

    Virus-induced apoptosis of infected cells can limit both the time and the cellular machinery available for virus replication. Hence, many viruses have evolved strategies to specifically inhibit apoptosis. However, Aleutian Mink Disease parvovirus (ADV) is the first example of a DNA virus that not only induces apoptosis but also utilizes caspase activity to facilitate virus replication. To determine the function of caspase activity during ADV replication, virus-infected cell lysates or purified ADV proteins were incubated with various purified caspases. Caspases cleaved the major nonstructural protein of ADV (NS1) at two caspase recognition sequences, whereas ADV structural proteins could not be cleaved. Importantly, the NS1 products could be identified in ADV-infected cells but were not present in infected cells pretreated with caspase inhibitors. By mutating putative caspase cleavage sites (D to E), we mapped the two cleavage sites to amino acid residues NS1:227 (INTD↓S) and NS1:285 (DQTD↓S). Replication of ADV containing either of these mutations was reduced 103- to 104-fold compared to that of wild-type virus, and a construct containing both mutations was replication defective. Immunofluorescent studies revealed that cleavage was required for nuclear localization of NS1. The requirement for caspase activity during permissive replication suggests that limitation of caspase activation and apoptosis in vivo may be a novel approach to restricting virus replication.

  • Caspase Activation Is Required for Permissive Replication of Aleutian Mink Disease Parvovirus in Vitro
    Virology, 2002
    Co-Authors: Sonja M. Best, James B. Wolfinbarger, Marshall E. Bloom
    Abstract:

    Abstract Aleutian Mink Disease parvovirus (ADV) is distinct among the parvoviruses as infection in vivo is persistent, restricted, and noncytopathic. In contrast, infections with other more prototypic parvoviruses, like Mink enteritis virus (MEV), are acute, cytopathic, and characterized by permissive replication in vivo. Although apoptosis results in the death of cells acutely infected by parvoviruses, the role of apoptosis in ADV infections is unknown. Permissive infection of ADV resulted in apoptosis of Crandell feline kidney (CrFK) cells as indicated by TUNEL staining, Annexin-V staining, and characteristic changes in cell morphology. Pretreatment of infected cells with caspase 3 or broad-spectrum caspase inhibitors prevented apoptosis. In addition, treatment of infected cells with these inhibitors caused a 2 log 10 reduction in the yield of infectious virus compared to untreated cultures. This block in replication preceded substantial viral DNA amplification and gene expression. However, inhibitors of caspases 1, 6, and 8 did not have this effect. MEV also induced caspase-dependent apoptosis following infection of CrFK cells, although production of infectious progeny was not affected by inhibition of apoptosis. Thus, permissive replication of ADV in vitro depended upon activation of specific caspases. If ADV infection of cells in vivo fails to initiate caspase activation, the requirement of caspase activity for replication may not be met, thus providing a possible mechanism for persistent, restricted infection.

  • Aleutian Mink Disease parvovirus in wild riparian carnivores in Spain.
    Journal of wildlife diseases, 2001
    Co-Authors: Sisco Mañas, James B. Wolfinbarger, Juan Carlos Ceña, Jordi Ruiz-olmo, Santiago Palazón, Mariano Domingo, Marshall E. Bloom
    Abstract:

    Serious declines in populations of native European Mink (Mustela lutreola) have occurred in Europe. One responsible factor may be infectious Diseases introduced by exotic American Mink (Mustela vison). In order to investigate a possible role for Aleutian Mink Disease parvovirus (ADV), we surveyed native riparian carnivores and feral American Mink. When serum samples from 12 free-ranging European and 16 feral American Mink were tested, antibodies to ADV were detected from three of nine European Mink. ADV DNA was detected by polymerase chain reaction in whole cell DNA from four of seven carcasses; two American Mink, one European Mink and a Eurasian otter (Lutra lutra). Lesions typical of Aleutian Disease were present in one of the American Mink. A portion of the ADV VP2 capsid gene was sequenced and the results suggested that two sequence types of ADV were circulating in Spain, and that the Spanish ADVs differed from other described isolates from North America and Europe. Future conservation and restoration efforts should include measures to avoid introduction or spread of ADV infection to native animals.

Bent Aasted – One of the best experts on this subject based on the ideXlab platform.

  • DISPATCHES Aleutian Mink Disease Virus and Humans
    , 2013
    Co-Authors: Jørgen R. Jepsen, Michael Roost Clausen, Elisabeth Gottschalck, Bent Aasted
    Abstract:

    Reports of a possible relationship between Aleutian Mink Disease parvovirus (AMDV) and human infection are rare. However, 2 Mink farmers with vascular Disease and microangiopathy similar to that in Mink with Aleutian Disease were found to have AMDV-specifi c antibodies and AMDV DNA. These fi ndings raise the suspicion that AMDV may play a role in human Disease. Autonomous parvoviruses, such as Aleutian Mink Disease virus (AMDV), cause a broad spectrum of Diseases in animals and man. Acute Disease manifests itself as a lytic infection of rapidly dividing cells; chronic Disease reflects a restricted or abortive infection of specific cell types (1). Aleutian Disease (AD) is known to produce clinical signs in Mink and ferrets only (2,3), although other mammals have reportedly been antibody positive

  • Aleutian Mink Disease virus and humans
    Emerging infectious diseases, 2009
    Co-Authors: Jørgen R. Jepsen, Michael Roost Clausen, Elisabeth Gottschalck, Francesco D'amore, Ulrik Baandrup, Bent Aasted
    Abstract:

    Reports of a possible relationship between Aleutian Mink Disease parvovirus (AMDV) and human infection are rare. However, 2 Mink farmers with vascular Disease and microangiopathy similar to that in Mink with Aleutian Disease were found to have AMDV-specific antibodies and AMDV DNA. These findings raise the suspicion that AMDV may play a role in human Disease.

  • Replication of Aleutian Mink Disease parvovirus in Mink lymph node histocultures.
    Microbiology, 2000
    Co-Authors: Klaus T. Jensen, Bent Aasted, James B. Wolfinbarger, Marshall E. Bloom
    Abstract:

    Aleutian Mink Disease parvovirus (ADV), causes an immune disorder with a persistent infection of lymphoid organs in adult Mink. We studied replication of ADV in gel-supported histocultures prepared from adult Mink mesenteric lymph node (MLN). Evidence of virus replication in the histocultures was first observed by indirect immunofluorescence 72 h after incubation with virus. Cells resembling lymphocytes and macrophages contained both ADV capsid (VP2) and nonstructural (NS1 and NS2) proteins, and were present in a distribution suggestive of infected cells within germinal centres. ADV replicative form and encapsidated virion DNA were also detected in infected histocultures at time-points after 72 h. In addition, we were able to passage ADV-Utah to a new round of histocultures. These results suggested that the infected cells were actual target cells for ADV replication and that productive ADV-Utah replication, complete with the generation of virus, was occurring in the histocultures. The Mink MLN histocultures provide a system to study the replication and molecular pathogenesis of ADV in target tissues.

Hongyan Chen – One of the best experts on this subject based on the ideXlab platform.

  • Aptamer-targeting of Aleutian Mink Disease virus (AMDV) can be an effective strategy to inhibit virus replication.
    Scientific reports, 2021
    Co-Authors: Hui Zhang, Lili Zhao, Wenzhuo Yan, Jie Zhou, Hongyan Chen
    Abstract:

    Aleutian Mink Disease (AMD), which is caused by Aleutian Mink Disease virus (AMDV), is an important contagious Disease for which no effective vaccine is yet available. AMD causes major economic losses for Mink farmers globally and threatens some carnivores such as skunks, genets, foxes and raccoons. Aptamers have exciting potential for the diagnosis and/or treatment of infectious viral Diseases, including AMD. Using a magnetic beads-based systemic evolution of ligands by exponential enrichment (SELEX) approach, we have developed aptamers with activity against AMDV after 10 rounds of selection. After incubation with the ADVa012 aptamer (4 μM) for 48 h, the concentration of AMDV in the supernatant of infected cells was 47% lower than in the supernatant of untreated cells, whereas a random library of aptamers has no effect. The half-life of ADVa012 was ~ 32 h, which is significantly longer than that of other aptamers. Sequences and three dimensions structural modeling of selected aptamers indicated that they fold into similar stem-loop structures, which may be a preferred structure for binding to the target protein. The ADVa012 aptamer was shown to have an effective and long-lasting inhibitory effect on viral production in vitro.

  • Development of an antigen-capture enzyme-linked immunosorbent assay for diagnosis of Aleutian Mink Disease virus.
    Archives of virology, 2020
    Co-Authors: Yuanzhi Wang, Lili Zhao, Hongyan Chen
    Abstract:

    Aleutian Mink Disease (AMD), caused by Aleutian Mink Disease virus (AMDV), is a very important infectious Disease of Mink. Currently, elimination of antibody– or antigen-positive animals is the most successful strategy for eradicating AMD, but the claw-cutting method of blood sampling is difficult to perform and painful for the animal. In this study, we aimed to establish an antigen capture enzyme-linked immunosorbent assay (AC-ELISA) method for the efficient detection of AMDV antigens using fecal samples. A purified mouse monoclonal antiantibody (mAb) was used as the capture antibody, and a rabbit polyclonal antibody (pAb) was used as the detection antibody. The assay was optimized by adjusting a series of parameters. Using a cutoff value of 0.205, the limit of detection of the AC-ELISA for strain AMDV-G antigen was 2 μg/mL, and there was no cross-reaction with other Mink viruses. The intra- and inter-assay standard deviations were below 0.046, and the correlation of variance (CV) values were 1.24-7.12% when testing fecal samples. Compared with conventional PCR results, the specificity and sensitivity were 91.5% and 90.6%, respectively, and the concordance rate between the two methods was 91.1%.

  • Identification and characterization of a novel B-cell epitope on Aleutian Mink Disease virus capsid protein VP2 using a monoclonal antibody.
    Virus research, 2017
    Co-Authors: Yuanzhi Wang, Wenzhuo Yan, Yuanyuan Zhang, Lili Zhao, Hongyan Chen
    Abstract:

    Abstract Aleutian Mink Disease is caused by a highly contagious parvovirus (Aleutian Mink Disease virus, AMDV). This Disease is one of the most commercially important infectious Disease worldwide and causes considerable economic losses to Mink farmers. The capsid protprotein VP2 is the major immunogenic antigenic protein of AMDV, and is involved in viral tropism, pathogenicity, and host selection. However, few reports have described the use of VP2-specific monoclonal antibodies (mAbs) in B-cell epitope identification and immunological detection. In this study, we produced a specific mAb, 1G5, against AMDV VP2 protein (amino acids: 200 ∼ 588) and characterized its specificity and relative affinity. Six partially overlapping truncated recombinant proteins and seven synthetized peptides were used to identify the epitopes recognized by 1G5. The results indicate that mAb 1G5 can distinguish AMDV, MEV and CPV2 with high affinity (Ka = 5.37 × 109), and the minimal linear epitope is located in amino acid residues 459EEEGWPAASGTHFED473. Sequence alignments demonstrated that the linear epitope was completely conserved among most Amdoparvoviruses except the bat parvovirus, where three substitutions (463W-463F, 466A-466G and 471F-471Y) were noted. Our results reveal that the identified epitope might be a common B-cell epitope of AMDV antibodies, and the 1G5 mAb can be used to identify the cleavage of the capsid proteins during AMDV infection. This is also the first report of a B-cell epitope on AMDV capsid protprotein VP2 (VP2: 459–473) using a mAb. These findings have potential applications in the development of new diagnostic tools for AMDV.

Soren Alexandersen – One of the best experts on this subject based on the ideXlab platform.

  • s phase dependent cell cycle disturbances caused by Aleutian Mink Disease parvovirus
    Journal of Virology, 1997
    Co-Authors: Martin B. Oleksiewicz, Soren Alexandersen
    Abstract:

    We examined replication of the autonomous parvovirus Aleutian Mink Disease parvovirus (ADV) in relation to cell cycle progprogression of permissive Crandell feline kidney (CRFK) cells. Flow cytometric analysis showed that ADV caused a composite, binary pattern of cell cycle arrest. ADV-induced cell cycle arrest occurred exclusively in cells containing de novo-synthesized viral nonstructural (NS) proteins. Production of ADV NS proteins, indicative of ADV replication, was triggered during S-phase traverse. The NS+ cells that were generated during later parts of S phase did not undergo cytokinesis and formed a distinct population, termed population A. Formation of population A was not prevented by VM-26, indicating that these cells were arrested in late S or G2 phase. Cells in population A continued to support high-level ADV DNA replication and production of infectious virus after the normal S phase had ceased. A second, postmitotic, NS+ population (termed population B) arose in G0/G1, downstream of population A. Population B cells were unable to traverse S phase but did exhibit low-level DNA synthesis. Since the nature of this DNA synthesis was not examined, we cannot at present differentiate between G1 and early S arrest in population B. Cells that became NS+ during S phase entered population A, whereas population B cells apparently remained NS- during S phase and expressed high NS levels postmitosis in G0/G1. This suggested that population B resulted from leakage of cells with subthreshold levels of ADV products through the late S/G2 block and, consequently, that the binary pattern of ADV-induced cell cycle arrest may be governed merely by viral replication levels within a single S phase. Flow cytometric analysis of propidium iodiiodide fluorescence and bromodeoxyuridine uptake showed that population A cells sustained significantly higher levels of DNA replication than population B cells during the ADV-induced cell cycle arrest. Therefore, the type of ADV-induced cell cycle arrest was not trivial and could have implications for subsequent viral replication in the target cell.

  • Subcellular localization of Aleutian Mink Disease parvovirus proteins and DNA during permissive infection of Crandell feline kidney cells.
    Journal of virology, 1996
    Co-Authors: Martin B. Oleksiewicz, James B. Wolfinbarger, Fred Costello, Mark E. Huhtanen, Soren Alexandersen, Marshall E. Bloom
    Abstract:

    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 formed hollow 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.

  • Investigation of the pathogenesis of transplacental transmission of Aleutian Mink Disease parvovirus in experimentally infected Mink.
    Journal of virology, 1996
    Co-Authors: Susanne Broll, Soren Alexandersen
    Abstract:

    The transplacental transmission of Aleutian Mink Disease parvovirus (ADV) was studied in experimental infection of 1-year-old female non-Aleutian Mink. The ADV-seronegative female Mink were inoculated with ADV prior to mating or after the expected implantation of the embryos during pregnancy. A group of uninfected females served as a control group. Animals from each group were killed prior to or shortly after parturition. The in situ hybridization technique with radiolabeled strand-specific RNA probes was used to determine target cells of virus infection and virus replication. In both infected groups, ADV crossed the endotheliochorial placental barrier, although animals infected before mating already had high antibody titers against ADV at the time of implantation. The percentage of dead and resorbed fetuses was much higher in dams infected before mating. In the placentae of these Mink, virus DNA and viral mRNA were detected in cells in the mesenchymal stroma of the placental labyrinth and hematoma but only occasionally in the cytotrophoblast of the placental hematoma. Placentae of animals infected during pregnancy showed in addition very high levels of virus and also viral replication in a large number of cytotrophoblast cells in the placental hematoma, which exhibited distinct inclusion bodies. In both groups, neither virus nor virus replication could be detected in maternal endothelial cells or fetal syncytiotrophoblast of the placental labyrinth. Fetuses were positive for virus and viral replication at high levels in a wide range of tissues. Possible routes of transplacental transmission of ADV and the role of trophoblast cells as targets for viral replication are discussed. Aleutian Mink Disease parvovirus (ADV) in adult Mink causes a persistent infection usually followed by a chronic, progressive Disease associated with a disorder of the immune system (2, 19, 33, 34, 36, 39), which is characterized by the development of plasmacytosis, hypergammaglobulinemia, and immune complex-mediated glomerulonephritis and arteritis in the chronic stage of the Disease. Viral replication was demonstratedinlymphaticorgans,withapeak10daysafterinfection, but then rapidly decreased, and by 60 days after infection, viral replication was below detectable levels (2). InMinkkitsinfectedasnewborns,anacuteinterstitialpneu