Immune mediated and inherited defences against flaviviruses

Immune mediated and inherited defences against flaviviruses
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DOI:
10.1016/s0928-0197(98)00039-7
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发表时间:
1998-07-15
期刊:
CLINICAL AND DIAGNOSTIC VIROLOGY
影响因子:
--
通讯作者:
Ennis, FA
Ennis, FA
中科院分区:
其他
文献类型:
--
作者:
Brinton, MA;Kurane, I;Ennis, FA

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背景:黄病毒感染可引起机体产生针对多种病毒蛋白的免疫应答。对黄病毒诱导的疾病的抗性也可以通过涉及天然存在的鼠基因Flv的产物的非免疫机制来控制。目的:回顾已经报道了在小鼠或人类中引发T细胞或B细胞免疫应答的黄病毒蛋白上的表位的作图的研究,并讨论黄病毒特异性遗传抗性的可能机制。纯化的病毒蛋白和合成肽用于绘制B细胞表位。纯化的蛋白质、牛痘表达的病毒蛋白片段和合成肽用于绘制T细胞表位。结果:在几种黄病毒的E、NS1和NS3蛋白上分别定位了T细胞和B细胞抗原表位。对C、PreM、NS2a、NS4a和NS5蛋白的免疫应答也已被记录。数据表明,飞基因产物的细胞内抑制病毒基因组RNA.Conclusions的合成:虽然黄病毒感染elyphon丰富的免疫反应,这种反应并不总是足够快,以保护主机从发展脑炎。在继发性感染期间,体液和细胞黄病毒特异性反应都可以提供保护。登革出血热(DHF)和登革休克综合征(DSS)似乎是由过度强烈的免疫反应引起的。在具有遗传抗性的动物中,减少病毒的产生导致感染的传播较慢,这反过来又使免疫反应有时间发展并在疾病症状出现之前清除感染。(C)1998 Elsevier Science B.V.保留所有权利。
Background: Flavivirus infection elicits an abundant immune response in the host which is directed against a number of the viral proteins. Resistance to flavivirus-induced disease can also be controlled via a non-immune mechanism involving the product of a naturally occurring murine gene, Flv.Objectives: To review studies that have reported the mapping of epitopes on flavivirus proteins that elicit T- or B-cell immune responses in mice or humans and to discuss a possible mechanism for flavivirus-specific genetic resistance.Study design: Purified viral proteins and synthetic peptides were used to map B-cell epitopes. Purified proteins, vaccinia-expressed viral protein fragments and synthetic peptides were used to map T-cell epitopes. Congnic-resistant, C3H/RV and congenic susceptible, C3H/He mice and cell cultures were used to study the mechanism of genetic resistance to flavivirus infection.Results: T- and B-cell epitopes have been mapped to the E, NS1 and NS3 proteins of several flaviviruses. Immune responses to the C, PreM, NS2a, NS4a, and NS5 proteins have also been documented. Data suggest that the Fly gene product acts intracellularly to suppress the synthesis of viral genomic RNA.Conclusions: Although flavivirus infection elicits an abundant immune response, this response is not always rapid enough to protect the host from developing encephalitis. During secondary infections both the humoral and cellular flavivirus-specific responses can confer protection. Dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) appear to be caused by an overly vigorous immune response. In genetically resistant animals reduced production of virus results in a slower spread of the infection, which in turn allows time for the immune response to develop and to clear the infection before disease symptoms appear. (C) 1998 Elsevier Science B.V. All rights reserved.