水貂阿留申病毒结构蛋白与非结构蛋白在疾病诊断与疫苗研发中的应用

水貂阿留申病是由水貂阿留申病毒引起的一种持续感染性疾病,危害毛皮动物养殖业的发展.水貂阿留申病毒的致病特点、免疫机制等与其他细小病毒不同,存在自身的复杂性.目前,众多研究者寻求新的疫苗来预防水貂阿留申病的发生,但没有取得理想的效果.疾病诊断及疫苗研发对防控水貂阿留申病具有积极的意义.水貂阿留申病毒结构蛋白在病毒感染、机...     

水貂阿留申病病毒CIEP抗原结合蛋白初探

以水貂阿留申病病毒对流免疫电泳(CIEP)细胞抗原为材料,经酶印迹(Westemblotting)测定,水貂阿留申病病毒CIEI细胞抗原与多克隆阳性血清反应,分子量为60000,50000和25000,而与CIEP阴性的抗水貂阿留申病病毒的单克隆抗体(Y—2—9)反应,分子量为60000,50000.因此初步确定水貂阿留申病病毒CIEP细胞抗原决定族位于分子25000蛋白上.     

水貂阿留申病研究进展

主要对国内外阿留申病毒的分子生物学进展及阿留申病的病理进行了综述。     

水貂阿留申病的诊治

水貂阿留申病是由阿留申病病毒引起的一种传染病.该病毒属细小病毒科,在水貂中主要引发两种不同类型的疾病.成年水貂感染病毒后,表现出典型的水貂阿留申病,以体内产生高水平的血清丙种球蛋白,浆细胞增多,持续性病毒血症及由免疫复合物沉积引发的严重肾小球肾炎并伴有动脉炎、肝炎、卵巢炎或睾丸炎等主要症状.     

水貂阿留申病PPA-ELISA诊断方法的研究

用感染水貂阿留申病病毒G株(ADV-G)的猫肾传代细胞(CRFK)建立了检测水貂阿留申病病毒抗体的PPA-ELISA法。该方法敏感性高于CIEP 16倍,具有快速,准确的优点,可用于病原定位,是水貂阿留申病检疫和研究较为理想的方法.     

一例水貂阿留申病毒和伪狂犬病毒混合感染的诊断

为确定河北衡水某水貂养殖场水貂大批量死亡的原因,笔者对死亡水貂进行解剖,采集其肾脏、脾脏等组织器官,进行阿留申病毒(ADV)、伪狂犬病毒(PRV)、犬瘟热病毒(CDV)和传染性肝炎病毒(CAV-Ⅰ/Ⅱ)检测。结果:阿留申病毒和伪狂犬病毒检测结果阳性,犬瘟热病毒和传染性肝炎病毒检测结果阴性,说明该养殖场的水貂感染了阿留申病毒和伪狂犬病病毒,应及时对畜舍进行消毒,隔离和淘汰阳性水貂。     

5株水貂阿留申病毒的分离与鉴定

为给水貂阿留申病疫苗的研制奠定基础,对疑似感染阿留申病死亡的水貂内脏处理后,接种猫肾传代细胞（CRFK）分离病毒,并对分离的毒株进行PCR鉴定及动物回归试验。与此同时,首次应用免疫过氧化物酶单层细胞实验（IPMA）对所分离的水貂阿留申病毒进行TCID50的测定。结果成功分离并鉴定出5株水貂阿留申病毒株,分别命名为ADV-DL124、ADV-DL125、ADV-ZJ3、ADV-QD2、ADV-QD3,各分离株的TCID50分别为105.7TCID50/ml、105.0TCID50/ml、104.6 TCID50/mL、105.2 TCID50/mL、104.1 TCID50/mL。动物回归实验显示,所分离的病毒对水貂具有致病性,为水貂阿留申病毒强毒株。     

阿留申病研究进展报告

<正> 这个课题总的目的是详细阐明传染病病原体与使水貂保毒和发病的病毒宿主的相互关系。本年度的目标是确定水貂阿留申病毒(简称ADV)雪貂株的致病能力,完成雪貂阿留申病毒的细胞培养。我们通过实验室研究,发现214只商品雪貂中42％具有阿留申病毒抗体。获得抗体的雪貂与无抗体的雪貂相比,血清γ—球蛋白显著增加。然而,与水貂相比,雪貂γ—球蛋白的增加要少得多,少数传染的雪貂,γ—球蛋白只增加3倍多。雪貂阿留申病毒抗体的滴度,也大大低于水貂。     

水貂阿留申病研究现状

水貂阿留申病(ADM)又称浆细胞增多症(plas-macytasis),是一种由主要侵害水貂免疫细胞的阿留申病毒(ADMV)引起的,导致自身免疫系统     

水貂阿留申病的诊治

水貂阿留申病是由细小病毒科,细小病毒属的阿留申病毒引起的一种慢性、进行性传染病,蓝色和黄色彩貂发病率最高,标准黑貂和其他深色貂也时有发生.该病的特征为淋巴细胞系统性增生、浆细胞普遍性增生、肾小球肾盂肾炎、持续性病毒血症、动脉炎及肝炎.     

Characteristics of inapparent Aleutian disease virus infection in mink.

Inapparent of nonprogressive Aleutian disease virus (ADV) infection is a subclinical but persistent virus infection of mink. Mink with the inapparent type of ADV infection when subjected to stress did not develop the progessive form of the disease. However, when challenged with a large dose of the virus, these mink did develop progressive Aleutian disease indicating that they were not highly resistant to the virus. Sera of mink with either the progressive of the inapparent type of ADV infection did not neutralise the virus. The anti-ADV antibody activity in mink with inapparent type of ADV infection was in the IgG fraction of the serum the same as in mink with progressive Aleutian disease. These data indicate that the resistance of the mink with inapparent infection as compared to mink with progressive Aleutian disease was not due to a difference in the class of immunoglobulin response to the virus. However, mink with progressive Aleutian disease showed a greatly increased immunoglobulin response.     

Comparison of the lesions of Aleutian disease in mink and hypergammaglobulinemia in ferrets.

Gross and microscopic lesions of Aleutian disease (AD) in mink and hypergammaglobulinemia in ferrets were compared. Both conditions were characterized by widespread proliferation of plasma cells, but proliferation was more prominent in mink infected with AD. Arteritis did not occur in hypergammaglobulinemic ferrets. Minimal or no glomerular alterations occurred in infected ferrets, but were severe in mink infected with AD. Bile duct proliferation was more prominent in diseased mink. Tissue alterations suggested that AD in Aleutian genotype mink is more rapidly progressive than is AD in ferrets, causing overt clinical disease and death. In contrast, hypergammaglobulinemia in ferrets appeared to progress more slowly, with little clinical evidence of disease. This is probably the result of a paucity of glomerular lesions in ferrets. Possible mechanisms to explain the differences in the development of lesions are discussed.     

Transmission of Aleutian disease from mink with inapparent infections.

In apparent or nonprogressive Aleutian disease virus infection was considered a subclinical but persistent viral infection in which infected mink did not develop tissue lesions, hypergammaglobulinemia, or high antibody titers. Transmission of Aleutian disease virus from mink with this type of infection was measured. Mink with inapparent Aleutian disease appeared healthy and had normal gamma-globulin values, but were capable of transmitting the disease by direct and indirect horizontal contact. The risk of direct or indirect horizontal transmission from mink with inapparent infection was less than from mink with progressive Aleutian disease. Infection also was directly transmitted from the dam to the kits, but again the risk of infection from dams with inapparent infection was less than from dams with progressive Aleutian disease. Mink infected from their dams before weaning developed the disease more slowly than mink which became infected after weaning.     

Aleutian Disease of Mink: I. Evidence of its Viral Etiology *

A suspension of tissues from field cases of Aleutian disease was used successfully to reproduce the disease in Aleutian mink. Similarly, suspensions of diseased tissues from the experimentally infected mink were used to transmit the agent of Aleutian disease to both Aleutian mink and standard dark mink. Seitz and millipore filtrates prepared from these tissue suspensions were also infective; a suggestion that the etiologic agent is a virus. Genetic factors and hypersensitivity are discussed as possibly contributing to development of the disease.     

水貂阿留申病的研究进展

水貂阿留申病(Aleutian disease of mink,ADM)是由水貂阿留申病细小病毒(Aleutian mink disease parvovirus,AD-MV)引起的一种慢性、进行性传染病,一直是危害世界养貂业健康发展最重要的疫病之一。到目前为止,还没有疫苗可成功用于ADM的预防,也没有特异有效的治疗方法,唯一可行的防治方法就是通过多次特异性检疫,淘汰病貂,净化貂群。笔者对阿留申病的病原学、发病机制、防治措施等方面进行概述,为临床防治水貂阿留申病提供了理论基础。     

Histopathologic and immunohistochemical lesions in liver of mink infected with Aleutian disease virus

Parvovirus of Aleutian disease causes mainly damage to kidneys, but immune complexes deposition and damage may occur also in other organs. In mink farms of Latvia the liver dystrophy or hepatic lipidosis of mink is widely distributed. The goal of this study was to examine probability of liver damage and regeneration of mink infected with Aleutian disease virus. Liver injury was assessed histologically. The mink liver demonstrated inflammation of liver parenchyma and foci of fatty liver. In immunohistochemistry, during liver regeneration the matrix metalloproteinases MMP-9, vascular endothelial growth factor and beta-defensin 2 expressions were lower, but MMP-2 and nerve growth factor receptor p75 expression was increased.     

Detection of antibody in Aleutian disease of mink: comparison of enzyme-linked immunosorbent assay and counterimmunoelectrophoresis

Experiments were undertaken to investigate the potential of the enzyme-linked immunosorbent assay (ELISA) as a screening test for the diagnosis of the 2 known naturally occurring forms of Aleutian disease of mink. Anti-Aleutian disease virus (ADV) antibody activity was not detectable in the sera of mink with nonprogressive Aleutian disease despite the demonstration of antibody by counterimmunoelectrophoresis (CIEP) in the same sera. Anti-ADV antibody was detectable in 93% of sera from mink at various stages of experimentally induced progressive Aleutian disease. False-negative reactions occurred in sera which demonstrated high anti-ADV antibody titers by CIEP. As a consequence of the high prevalence of false-negative reactions, the ELISA was not considered to be an effective screening test. However, using CIEP as an indicator of ADV infection, the ELISA may be useful in differentiating mink with nonprogressive Aleutian disease from mink with progressive Aleutian disease.     

水貂阿留申病诊断抗原研究概述

近年来,随着水貂养殖行业的不断发展,一些疫病也成为了制约水貂养殖业发展的重要因素。水貂阿留申病作为毛皮动物的三大疫病之一(阿留申病、犬瘟热、病毒性肠炎),是导致母貂产仔率下降、公貂配种能力降低和毛皮质量下降的一种高度接触性传染病。至今为止,还没有商品化的疫苗来控制该病的传播及蔓延。控制水貂阿留申病最好的方法是通过检测淘汰所有抗体为阳性的水貂,进而达到净化貂群的目的。而在抗体检测过程中,诊断抗原的制备和纯化决定着检测方法的敏感性、特异性和准确性。论文对目前阿留申病毒细胞抗原及基因工程抗原研究进展做一综述,为今后该病病原检测工作提供参考。     

水貂阿留申病发病机理的研究进展

水貂阿留申病是由阿留申病病毒引起的一种可对水貂养殖业造成严重损失的传染病。该病困扰动物医学界多年 ,始终未得到攻克。近年来随着分子生物学技术的发展 ,国内外学者对该病分子水平的发病机理有了更多的认识 ,研究内容主要集中在与水貂阿留申病发病密切相关的抗病毒抗体、病毒核酸的晚启动子P3 6及其顺式作用元件(cis acting)、结构蛋白VP2等方面。文章对以上研究进展进行了详细的归纳总结与分析 ,并在此基础上提出了尝试使用反义RNA或干扰RNA对该病进行预防、治疗的设想 ,以期今后对阿留申病的继续深入研究能有所帮助。