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受体小马的马传染性贫血病毒(EIAV)体液反应及持续感染期间的抗原变异

Equine infectious anemia virus (EIAV) humoral responses of recipient ponies and antigenic variation during persistent infection.

作者信息

Rwambo P M, Issel C J, Adams W V, Hussain K A, Miller M, Montelaro R C

机构信息

Department of Veterinary Microbiology and Parasitology, Louisiana State University, School of Veterinary Medicine, Baton Rouge.

出版信息

Arch Virol. 1990;111(3-4):199-212. doi: 10.1007/BF01311054.

DOI:10.1007/BF01311054
PMID:2162160
Abstract

Three ponies were inoculated with plasma containing 10(4.8) TCID50 of equine infectious anemia virus (EIAV) and observed for 165 to 440 days. Each pony developed a febrile response within 3 weeks of infection during which a plasma viremia greater than or equal to 10(3.5) TCID50/ml was observed. Analyses of four isolates from sequential febrile episodes in a single pony were conducted by two-dimensional tryptic peptide maps and with monoclonal antibodies in immunoblots. Structural and antigenic alterations were observed in the envelope glycoproteins gp90 and gp45, with greatest variation in gp90. Specific IgG to EIAV gp90, gp45, and p26 of homologous and heterologous isolates was detectable by immunoblots within one month after infection although IgG levels to gp45 at this time were relatively low. The group-specific determinants of gp90 and gp45 were more antigenic than those of p26; however, binding of IgG to these determinants did not correlate with neutralization of EIAV as assayed in fetal equine kidney cells. Neutralizing antibodies were first detectable within two months of infection and only neutralized viruses isolated prior to serum collection. Neutralizing activity of sera collected later in the infection was broadly reactive regardless of the number of clinical episodes the donor had suffered.

摘要

三只小马接种了含有10(4.8) 半数组织培养感染剂量(TCID50)马传染性贫血病毒(EIAV)的血浆,并观察了165至440天。每只小马在感染后3周内出现发热反应,在此期间观察到血浆病毒血症大于或等于10(3.5) TCID50/ml。通过二维胰蛋白酶肽图谱和免疫印迹中的单克隆抗体,对一匹小马连续发热发作的四个分离株进行了分析。在包膜糖蛋白gp90和gp45中观察到结构和抗原性改变,其中gp90变化最大。感染后一个月内,通过免疫印迹可检测到针对同源和异源分离株的EIAV gp90、gp45和p26的特异性IgG,尽管此时针对gp45的IgG水平相对较低。gp90和gp45的群特异性决定簇比p26的更具抗原性;然而,IgG与这些决定簇的结合与在马胎儿肾细胞中测定的EIAV中和作用不相关。中和抗体在感染后两个月内首次可检测到,并且仅中和血清采集前分离的病毒。感染后期采集的血清的中和活性具有广泛的反应性,无论供体经历的临床发作次数如何。

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1
Equine infectious anemia virus (EIAV) humoral responses of recipient ponies and antigenic variation during persistent infection.受体小马的马传染性贫血病毒(EIAV)体液反应及持续感染期间的抗原变异
Arch Virol. 1990;111(3-4):199-212. doi: 10.1007/BF01311054.
2
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An EIAV field isolate reveals much higher levels of subtype variability than currently reported for the equine lentivirus family.

本文引用的文献

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Isolation of equine infectious anemia virus glycoproteins. Lectin affinity chromatography procedures for high avidity glycoproteins.马传染性贫血病毒糖蛋白的分离。用于高亲和力糖蛋白的凝集素亲和层析程序。
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Virulence and in vitro growth of a cell-adapted strain of equine infectious anemia virus after serial passage in ponies.马传染性贫血病毒细胞适应株在小马体内连续传代后的毒力及体外生长情况
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"Western blotting": electrophoretic transfer of proteins from sodium dodecyl sulfate--polyacrylamide gels to unmodified nitrocellulose and radiographic detection with antibody and radioiodinated protein A.
一株 EIAV 野外分离株显示出比目前报道的马属慢病毒科更高水平的亚型变异性。
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Discerning an effective balance between equine infectious anemia virus attenuation and vaccine efficacy.在马传染性贫血病毒减毒与疫苗效力之间找到有效的平衡。
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5
CTL from EIAV carrier horses with diverse MHC class I alleles recognize epitope clusters in Gag matrix and capsid proteins.来自具有不同MHC I类等位基因的马传染性贫血病毒(EIAV)携带者马匹的细胞毒性T淋巴细胞(CTL)识别Gag基质蛋白和衣壳蛋白中的表位簇。
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6
Adaptive immunity is the primary force driving selection of equine infectious anemia virus envelope SU variants during acute infection.适应性免疫是急性感染期间驱动马传染性贫血病毒包膜SU变体选择的主要力量。
J Virol. 2004 Sep;78(17):9295-305. doi: 10.1128/JVI.78.17.9295-9305.2004.
7
Epitope specificity is critical for high and moderate avidity cytotoxic T lymphocytes associated with control of viral load and clinical disease in horses with equine infectious anemia virus.表位特异性对于与马传染性贫血病毒感染马的病毒载量控制和临床疾病相关的高亲和力和中等亲和力细胞毒性T淋巴细胞至关重要。
Virology. 2003 Sep 1;313(2):537-52. doi: 10.1016/s0042-6822(03)00344-1.
8
A live attenuated equine infectious anemia virus proviral vaccine with a modified S2 gene provides protection from detectable infection by intravenous virulent virus challenge of experimentally inoculated horses.一种带有修饰S2基因的马传染性贫血病毒减毒活前病毒疫苗,可保护经实验接种的马匹免受静脉注射强毒病毒攻击后可检测到的感染。
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Equine infectious anemia virus envelope evolution in vivo during persistent infection progressively increases resistance to in vitro serum antibody neutralization as a dominant phenotype.马传染性贫血病毒在持续感染期间体内包膜的进化逐渐增加对体外血清抗体中和的抗性,这是一种主要表型。
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Immune responses and viral replication in long-term inapparent carrier ponies inoculated with equine infectious anemia virus.接种马传染性贫血病毒的长期隐性携带小马的免疫反应和病毒复制
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“蛋白质免疫印迹法”:蛋白质从十二烷基硫酸钠 - 聚丙烯酰胺凝胶电泳转移至未修饰的硝酸纤维素膜上,并用抗体和放射性碘化蛋白A进行放射自显影检测。
Anal Biochem. 1981 Apr;112(2):195-203. doi: 10.1016/0003-2697(81)90281-5.
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Equine infectious anemia virus, a putative lentivirus, contains polypeptides analogous to prototype-C oncornaviruses.马传染性贫血病毒,一种假定的慢病毒,含有与原型C型肿瘤病毒类似的多肽。
Virology. 1980 Dec;107(2):520-5. doi: 10.1016/0042-6822(80)90319-0.
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Genomic changes associated with antigenic variation of visna virus durig persistent infection.与维斯纳病毒持续感染期间抗原变异相关的基因组变化。
Proc Natl Acad Sci U S A. 1980 Aug;77(8):4454-8. doi: 10.1073/pnas.77.8.4454.
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Antigenic variation during persistent infection by equine infectious anemia virus, a retrovirus.马传染性贫血病毒(一种逆转录病毒)持续感染期间的抗原变异
J Biol Chem. 1984 Aug 25;259(16):10539-44.
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Isolation and comparative biochemical properties of the major internal polypeptides of equine infectious anemia virus.马传染性贫血病毒主要内部多肽的分离及比较生化特性
J Virol. 1982 Jun;42(3):1029-38. doi: 10.1128/JVI.42.3.1029-1038.1982.
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Genomic alterations associated with persistent infections by equine infectious anaemia virus, a retrovirus.
J Gen Virol. 1984 Aug;65 ( Pt 8):1395-9. doi: 10.1099/0022-1317-65-8-1395.
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Cleavage of structural proteins during the assembly of the head of bacteriophage T4.在噬菌体T4头部组装过程中结构蛋白的切割
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10
Production of equine infectious anemia antigen in a persistently infected cell line.在持续感染的细胞系中生产马传染性贫血抗原。
Arch Gesamte Virusforsch. 1973;42(4):361-70. doi: 10.1007/BF01250717.