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Identification of a nonproductive, cell-associated form of measles virus by its resistance to inhibition by recombinant human interferon.

机译:通过其对重组人干扰素的抗性抗性鉴定非培养,细胞相关形式的麻疹病毒。

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Subacute sclerosing panencephalitis (SSPE) is a fatal disease in children and young adults that is caused by persistent infection of the central nervous system (CNS) by a nonproductive, cell-associated form of measles virus. Using an experimental model for SSPE (LEC viral strain in newborn hamsters), we have shown previously that establishment of such CNS infections involves selective elimination from the CNS of productively infected cells by host defensive mechanisms, coupled with the selective sparing of cells carrying nonproductive viral forms. That interferon (IFN) may play a role in this process was suggested by the disappearance of productively infected cells from the CNS tissues prior to the appearance of antiviral antibodies and by the demonstration of cell-associated, IFN-resistant viral variants in the virus stocks that were used. Results of this study support these conclusions by showing that similar IFN-resistant viral variants are present in the HBS strain of SSPE-derived measles virus and that these variants, in the presence of IFN, have properties that are similar to those of naturally occurring cell-associated strains of SSPE viruses, e.g., DR, IP3, and Biken. These IFN-resistant forms of HBS virus were isolated and were shown to maintain their resistance to inhibition by IFN after cloning. However, on removal of IFN, they reverted to productive forms similar to the parental HBS virus. The potential role of such viral forms in the pathogenesis of SSPE is discussed.
机译:亚急性硬化的终连脑炎(SSPE)是儿童和年轻成年人的致命疾病,这是由非营发布的细胞相关的麻疹病毒的中枢神经系统(CNS)持续感染引起的。利用SSPE的实验模型(新生儿仓鼠中的LEC病毒菌株),我们以前表明,这种CNS感染的建立涉及通过宿主防御机制从高效的细胞的CNS选择性消除,同时加上携带非培养性病毒的细胞的选择性备注形式。干扰素(IFN)可能在该过程中发挥作用,提出了在抗病毒抗体外出现之前从CNS组织的有效感染细胞的消失,并通过病毒股中的细胞相关的,IFN抗性病毒变体的示范性使用。本研究的结果通过表明,SSPE衍生的麻疹病毒HBS菌株中存在类似的IFN抗性病毒变体,并且这些变体在IFN存在下具有与天然存在的细胞类似的性质 - SSPE病毒的菌株,例如,DR,IP3和Biken。分离出这些IFN抗性的HBS病毒,并显示其在克隆后通过IFN保持其对抑制作用的抗性。然而,在去除IFN时,它们恢复为类似于亲本HBS病毒的生产形式。讨论了这种病毒形式在SSPE发病机制中的潜在作用。

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