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灭活全病毒疫苗和亚单位疫苗在预防马传染性贫血病毒引起的感染和疾病方面的效果。

Efficacy of inactivated whole-virus and subunit vaccines in preventing infection and disease caused by equine infectious anemia virus.

作者信息

Issel C J, Horohov D W, Lea D F, Adams W V, Hagius S D, McManus J M, Allison A C, Montelaro R C

机构信息

Department of Veterinary Science, Louisiana Agricultural Experiment Station, Baton Rouge.

出版信息

J Virol. 1992 Jun;66(6):3398-408. doi: 10.1128/JVI.66.6.3398-3408.1992.

Abstract

We report here on a series of vaccine trials to evaluate the effectiveness of an inactivated equine infectious anemia virus (EIAV) whole-virus vaccine and of a subunit vaccine enriched in EIAV envelope glycoproteins. The inactivated vaccine protected 14 of 15 immunized ponies from infection after challenge with at least 10(5) 50% tissue culture-infective doses of the homologous prototype strain of EIAV. In contrast, it failed to prevent infection in any of 15 immunized ponies that were challenged with the heterologous PV strain. Levels of PV virus replication and the development of disease, however, were significantly reduced in 12 of the 15 ponies so challenged. The subunit vaccine prevented infection from homologous challenge in four of four ponies tested but failed to prevent infection in all four challenged with the PV strain. Two of the four subunit vaccinates had more severe symptoms of equine infectious anemia than nonimmunized ponies infected in parallel. Both vaccines stimulated EIAV-specific cell-mediated immunity. The in vitro lymphoproliferative response was shown to be mediated by T lymphocytes and appeared to be indistinguishable from that induced by EIAV infection. Significant differences were observed in the in vivo lymphocyte responses following challenge with the two virus strains. While peripheral blood mononuclear cells from the inactivated virus vaccinates were equally stimulated by both the prototype and PV strains, the subunit vaccinates challenged with PV exhibited lower levels of spontaneous proliferation and serine esterase activity. This diminished cellular response to PV was correlated with more severe clinical disease in the same ponies. These studies demonstrate for the first time that both an EIAV inactivated whole-virus vaccine and a viral envelope glycoprotein-based subunit vaccine can provide protection against rigorous challenge levels of homologous virus but are unable to protect against similar challenge levels of a heterologous virus. Moreover, the data demonstrate that protection can be achieved in the absence of detectable levels of virus-specific neutralizing antibody in the vaccine recipients at the time of virus challenge. While vaccine-induced virus-specific cell-mediated immune responses were detected, their role in conferring protection was not obvious. Nevertheless, protection from disease appeared to be correlated with the induction of high levels of serine esterase activity following challenge. A significant observation is that while the whole-virus vaccine was usually capable of preventing or markedly moderating disease in the PV-infected ponies, the subunit vaccine appeared to have a high potential to enhance the disease induced by PV infection.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

我们在此报告一系列疫苗试验,以评估一种灭活马传染性贫血病毒(EIAV)全病毒疫苗和一种富含EIAV包膜糖蛋白的亚单位疫苗的有效性。灭活疫苗保护了15匹免疫小马中的14匹,使其在受到至少10⁵个50%组织培养感染剂量的同源原型株EIAV攻击后未被感染。相比之下,在15匹用异源PV株攻击的免疫小马中,它未能预防任何一匹小马被感染。然而,在15匹受到如此攻击的小马中,有12匹小马的PV病毒复制水平和疾病发展程度显著降低。亚单位疫苗在4匹受试小马中预防了同源攻击导致的感染,但在所有4匹用PV株攻击的小马中未能预防感染。4匹接种亚单位疫苗的小马中有2匹出现了比平行感染的未免疫小马更严重的马传染性贫血症状。两种疫苗都刺激了EIAV特异性细胞介导的免疫反应。体外淋巴细胞增殖反应显示由T淋巴细胞介导,并且似乎与EIAV感染诱导的反应没有区别。在用两种病毒株攻击后,在体内淋巴细胞反应中观察到了显著差异。虽然来自灭活病毒疫苗接种小马的外周血单核细胞受到原型株和PV株的同等刺激,但用PV攻击的亚单位疫苗接种小马表现出较低水平的自发增殖和丝氨酸酯酶活性。这种对PV的细胞反应减弱与同一批小马中更严重的临床疾病相关。这些研究首次证明,EIAV灭活全病毒疫苗和基于病毒包膜糖蛋白的亚单位疫苗都可以提供针对同源病毒严格攻击水平的保护,但无法针对异源病毒的类似攻击水平提供保护。此外,数据表明,在病毒攻击时,疫苗接种者体内不存在可检测水平的病毒特异性中和抗体的情况下也可以实现保护。虽然检测到了疫苗诱导的病毒特异性细胞介导的免疫反应,但其在提供保护方面的作用并不明显。然而,免受疾病侵害似乎与攻击后高水平丝氨酸酯酶活性的诱导相关。一个重要的观察结果是,虽然全病毒疫苗通常能够预防或显著减轻PV感染小马的疾病,但亚单位疫苗似乎有很高的可能性增强PV感染诱导的疾病。(摘要截短至400字)

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本文引用的文献

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Equine infectious anemia.马传染性贫血
Prog Med Virol. 1974;18(0):143-59.
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