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Application of real-time PCR to detect Aleutian Mink Disease Virus on environmental farm sources.

https://arctichealth.org/en/permalink/ahliterature262977
Source
Vet Microbiol. 2014 Oct 10;173(3-4):355-9
Publication Type
Article
Date
Oct-10-2014
Author
Alberto Prieto
José Manuel Díaz-Cao
Ricardo Fernández-Antonio
Rosario Panadero
Pablo Díaz
Ceferino López
Patrocinio Morrondo
Pablo Díez-Baños
Gonzalo Fernández
Source
Vet Microbiol. 2014 Oct 10;173(3-4):355-9
Date
Oct-10-2014
Language
English
Publication Type
Article
Keywords
Aleutian Mink Disease - epidemiology - genetics
Aleutian Mink Disease Virus - genetics - isolation & purification
Animals
Environmental Monitoring - methods
Mink
Real-Time Polymerase Chain Reaction - methods - veterinary
Regression Analysis
Spain - epidemiology
Abstract
The Aleutian Mink Virus (AMDV) causes the Aleutian Mink Disease (AMD) or Mink Plasmacytosis, a disease responsible of high economic losses for industry worldwide. Despite there is evidence of the environmental persistence of the virus, there is not literature on the detection of this virus in environmental samples in farms and this fact would have great importance in the control programs of the disease. In order to detect contamination caused by AMDV on farms, several environmental samples were taken and examined using qPCR. 93.9% of samples taken from farms confirmed to be infected tested positive. The virus was also detected on a farm which, despite having no previous positive results, was sharing personnel with an infected farm. All samples taken from AMD-free farms tested negative, including a farm where an eradication procedure by stamping out had been performed during the preceding months. Higher contamination levels were observed in samples from those surfaces in direct contact with animals. These results are the first demonstration of environmental contamination in farms, hitherto suggested by epidemiological evidences, caused by AMDV on surfaces, furniture and equipments inside mink farms. qPCR is an useful tool for evaluating the spread of AMDV into the environment, and it may have important applications within the disease control programs.
PubMed ID
25183237 View in PubMed
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Source
Cancer Invest. 1996;14(3):225-30
Publication Type
Article
Date
1996
Author
S E Erdman
P J Kanki
F M Moore
S A Brown
T A Kawasaki
K W Mikule
K U Travers
S F Badylak
J G Fox
Author Affiliation
Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge 02139, USA.
Source
Cancer Invest. 1996;14(3):225-30
Date
1996
Language
English
Publication Type
Article
Keywords
Aleutian Mink Disease Virus - genetics
Animals
Base Sequence
DNA Primers - chemistry
DNA, Viral - analysis
Disease Outbreaks
Ferrets
Leukemia Virus, Feline - genetics
Lymphoma - epidemiology - microbiology - veterinary
Molecular Sequence Data
Research Support, U.S. Gov't, P.H.S.
Abstract
Cluster outbreaks of lymphoma and leukemia have been associated with viral infections in many species including humans, cattle, and cats. This study describes epidemiological, clinical, and pathological features of cluster outbreaks of lymphoma in multiferret households and examines and compares the Aleutian disease virus (ADV) and feline leukemia virus (FeLV) status of cases, ferrets at risk, and controls. Three ferret groups with 21 cases of histologically diagnosed lymphoma (12.6% cumulative incidence) and their cohabitants (n = 35) were examined and compared with three control groups (n = 52) of cohabitating ferrets without lymphoma. A familial distribution was observed in one group but most cases were not consanguinous. Ferrets greater than 3 years of age developed chronic disease in two of the groups and 2-year-old adults had acute disease in the remaining group. Lymphocytosis, splenomegaly, and lymphadenopathy were prominent features. Histologically, predominantly small noncleaved cell and polymorphous lymphoid lesions were observed. All of the ferrets with lymphoma that were tested for ADV and FeLV using serology or PCR were negative. The rate of ADV antibody among cases or ferrets at risk was not significantly different from controls. None of the cluster ferrets were seropositive for FeLV p27 antigen using a monoclonal ELISA. Infection with a novel ferret virus is suspected, but an etiological agent has not yet been identified.
PubMed ID
8630683 View in PubMed
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Development and evaluation of a direct TaqMan qPCR assay for the rapid detection of diverse carnivore amdoparvoviruses.

https://arctichealth.org/en/permalink/ahliterature309972
Source
Mol Cell Probes. 2019 12; 48:101448
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
12-2019
Author
Yan-Hong Wu
Tao Wei
Xiu-Ting Zhang
Yong-Qiang Zhao
Jian-Ke Wang
Li Cong
Bao-Zeng Xu
Xi-Qun Shao
Author Affiliation
State Key Laboratory for Molecular Biology of Special Economic Animal, Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, 130112, China.
Source
Mol Cell Probes. 2019 12; 48:101448
Date
12-2019
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Aleutian Mink Disease Virus - genetics
Animals
DNA Primers - genetics
DNA, Viral - genetics
Dogs
Foxes - virology
Parvoviridae - genetics
Real-Time Polymerase Chain Reaction - methods
Reproducibility of Results
Sensitivity and specificity
Sequence Analysis, DNA - methods
Abstract
Amdoparvoviruses infect carnivore species, including mink, raccoon dog, fox, skunk, and red panda. Amdoparvovirus infection is a major cause of morbidity and mortality in farmed minks. Here, we developed a direct TaqMan qPCR assay for detection and quantification of carnivore amdoparvoviruses by using three primers and one probe based on the conserved VP2 gene. The detection limit for Aleutian mink disease virus (AMDV) and Raccoon dog and arctic fox amdoparvovirus (RFAV) were 4.06?×?101 copies/µl and 2.93?×?101 copies/µl, respectively. Both intra- and inter-assay variability were less than 2%. Among 74 carnivore samples, the positive rates for amdoparvoviruses were 62.2% (46/74) by direct TaqMan qPCR, while only 40.5% (30/74) by SYBR Green I qPCR. This result suggests that the direct TaqMan qPCR was more sensitive than the SYBR Green I qPCR. Additionally, the direct TaqMan qPCR is a rapid and sensitive method for liquid samples at microliter level as the assay employed the direct alkaline lysis method to obtain viral DNA and, therefore, eliminated the cumbersome steps in extracting DNA. Overall, the direct TaqMan qPCR assay possessed high specificity, sensitivity, and reproducibility, indicating that it can be used as a powerful tool for detection and quantification of various carnivore amdoparvoviruses in epidemiological and pathogenesis studies.
PubMed ID
31521579 View in PubMed
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[Eenie, Meenie, Miney, Moe, who is responsible for the antibody-dependent enhancement of Aleutian mink disease parvovirus infection?].

https://arctichealth.org/en/permalink/ahliterature257746
Source
Bing Du Xue Bao. 2014 Jul;30(4):450-5
Publication Type
Article
Date
Jul-2014
Author
Hong-Wei Zhu
Xiu-Mei Xing
Yong-Jun Wen
Source
Bing Du Xue Bao. 2014 Jul;30(4):450-5
Date
Jul-2014
Language
Chinese
Publication Type
Article
Keywords
Aleutian Mink Disease - immunology - virology
Aleutian Mink Disease Virus - genetics - immunology
Animals
Antibodies, Viral - immunology
Antibody-Dependent Enhancement
Mink - immunology - virology
Abstract
Aleutian mink disease parvovirus (AMDV) causes a persistent infection associated with immune complex disease, hypergammaglobulinemia, and high levels of antiviral antibodies. Despite the presence of an antibody, the virus is not cleared in vivo. Pre-existing antibodies may enhance viral infections, by Fc-receptor-mediated antibody-dependent enhancement (ADE), but the mechanism that underlies ADE has not been fully defined. Three models have been proposed, including: (1) interactions between antibody and FcR, complement C3 fragment and CR, or between C1q and C1qR, which promotes viral attachment to cells; (2) suppression of IFN-gamma-mediated host-cell antiviral gene expression by the upregulation of negative regulators of pathogen pattern recognition; and (3) the promotion of early IL-10 secretion. In addition, the role of cytokine IL-6 in ADE mediated disease development is discussed, to facilitate a better understanding of the pathogenesis of AMDV infection, as well as give insights into rational vaccine design approaches.
PubMed ID
25272602 View in PubMed
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Passive transfer of antiviral antibodies restricts replication of Aleutian mink disease parvovirus in vivo.

https://arctichealth.org/en/permalink/ahliterature5874
Source
J Virol. 1989 Jan;63(1):9-17
Publication Type
Article
Date
Jan-1989
Author
S. Alexandersen
S. Larsen
A. Cohn
A. Uttenthal
R E Race
B. Aasted
M. Hansen
M E Bloom
Author Affiliation
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.
Source
J Virol. 1989 Jan;63(1):9-17
Date
Jan-1989
Language
English
Publication Type
Article
Keywords
Acute Disease
Aleutian Mink Disease - prevention & control
Aleutian Mink Disease Virus - genetics - immunology - physiology
Animals
Antibodies, Viral - analysis
Chronic Disease
DNA, Viral - biosynthesis
Immunization, Passive - veterinary
Mink
Nucleic Acid Hybridization
Parvoviridae - immunology
Pulmonary Fibrosis - pathology - prevention & control - veterinary
Research Support, Non-U.S. Gov't
Viremia - veterinary
Virus Replication
Abstract
When mink kits were infected neonatally with a highly virulent strain of Aleutian disease virus (ADV), 100% of both Aleutian and non-Aleutian genotype mink died of interstitial pneumonia characterized by permissive ADV infection of alveolar type II cells. Treatment of infected kits with either mink anti-ADV gamma globulin or mouse monoclonal antibodies against ADV structural proteins reduced mortality by 50 to 75% and drastically reduced the severity of clinical signs. Interestingly, mink kits that survived the acute pulmonary disease all developed the chronic form of immune complex-mediated Aleutian disease. Thus, the antibodies directed against ADV structural proteins were capable of modulating the in vivo pathogenicity from an acute fulminant disease to a chronic immune complex-mediated disorder. The mechanism of this modulation was examined by strand-specific in situ hybridization. We found that the number of ADV-infected type II cells was the same in both untreated and antibody-treated kits. However, in the treated kits, viral replication and transcription were restricted at the cellular level. These data suggested that antibodies prevented acute viral pneumonia by restricting the intracellular level of viral replication and that the relevant antigenic determinants were contained within the viral structural proteins. The restricted levels of viral replication and transcription seen in antibody-treated mink kits resembled the levels observed in infected adult mink and suggested a role of antiviral antibodies in development of persistent infection and chronic immune complex disease.
PubMed ID
2535756 View in PubMed
Less detail

Role of alveolar type II cells and of surfactant-associated protein C mRNA levels in the pathogenesis of respiratory distress in mink kits infected with Aleutian mink disease parvovirus.

https://arctichealth.org/en/permalink/ahliterature59403
Source
J Virol. 1994 Apr;68(4):2720-5
Publication Type
Article
Date
Apr-1994
Author
B. Viuff
B. Aasted
S. Alexandersen
Author Affiliation
Department of Pharmacology and Pathobiology, Agricultural University of Copenhagen, Frederiksberg C, Denmark.
Source
J Virol. 1994 Apr;68(4):2720-5
Date
Apr-1994
Language
English
Publication Type
Article
Keywords
Aleutian Mink Disease - etiology
Aleutian Mink Disease Virus - genetics - growth & development
Animals
Animals, Newborn
DNA, Viral - isolation & purification
Humans
In Situ Hybridization
Infant, Newborn
Mink
Molecular Sequence Data
Proteolipids - biosynthesis - genetics
Pulmonary Alveoli - cytology - metabolism - microbiology
Pulmonary Surfactants - biosynthesis - genetics
RNA Probes
RNA, Messenger - isolation & purification
Research Support, Non-U.S. Gov't
Respiratory Distress Syndrome, Newborn - veterinary
Abstract
Neonatal mink kits infected with Aleutian mink disease parvovirus (ADV) develop an acute interstitial pneumonia with clinical symptoms and pathological lesions that resemble those seen in preterm human infants with respiratory distress syndrome and in human adults with adult respiratory distress syndrome. We have previously suggested that ADV replicates in the alveolar type II epithelial cells of the lung. By using double in situ hybridization, with the simultaneous use of a probe to detect ADV replication and a probe to demonstrate alveolar type II cells, we now confirm this hypothesis. Furthermore, Northern (RNA) blot hybridization showed that the infection caused a significant decrease of surfactant-associated protein C mRNA produced by the alveolar type II cells. We therefore suggest that the severe clinical symptoms and pathological changes characterized by hyaline membrane formation observed in ADV-infected mink kits are caused by a dysfunction of alveolar surfactant similar to that observed in respiratory distress syndrome in preterm infants. However, in the infected mink kits the dysfunction is due to the replication of ADV in the lungs, whereas the dysfunction of surfactant in preterm infants is due to lung immaturity.
PubMed ID
8139047 View in PubMed
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[Some molecular-biological and immunological aspects of Aleutian disease of mink]

https://arctichealth.org/en/permalink/ahliterature6704
Source
Zh Mikrobiol Epidemiol Immunobiol. 2002 Nov-Dec;(6):111-6
Publication Type
Article
Author
E B Faizuloev
Author Affiliation
Andzhaparidze Research Institute of Viral Preparations, Moscow, Russia.
Source
Zh Mikrobiol Epidemiol Immunobiol. 2002 Nov-Dec;(6):111-6
Language
Russian
Publication Type
Article
Keywords
Age Factors
Aleutian Mink Disease - genetics - immunology - virology
Aleutian Mink Disease Virus - genetics - immunology - pathogenicity
Animals
Antibodies, Viral - immunology
Antibody-Dependent Enhancement
B-Lymphocytes - immunology
Dendritic Cells - immunology
English Abstract
Gene Expression Regulation, Viral - immunology
Immunity, Cellular - physiology
Interleukin-6 - immunology
Macrophages - immunology
Mink
Promoter Regions (Genetics) - immunology
Abstract
Information on the development of the infectious process in the Aleutian disease of minks (ADM) on the molecular level, are updated. In particular, the decisive role played by the ABM virus infection of the cells of the immune system (B lymphocytes, macrophages, follicular dendritic cells) and the possible involvement of the mechanism of the antibody-dependent aggravation of this infection are pointed out. In addition, the role of the weak ADM virus promoter p36, the immune status of minks and their age in the determination of the acute or "slow" character of the course of the disease are considered.
PubMed ID
12506642 View in PubMed
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7 records – page 1 of 1.