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首页> 外文学位 >Interferons induce BST-2/tetherin in measles virus-infected neurons and permissive mice.
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Interferons induce BST-2/tetherin in measles virus-infected neurons and permissive mice.

机译：干扰素在麻疹病毒感染的神经元和宽容小鼠中诱导BST-2 /系膜蛋白。

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摘要

Though neurons can be productively infected with measles virus (MV), they do not display two of the cardinal hallmarks of peripheral infection: release of extracellular virions and associated cytopathicity due to syncytia formation. How neurons survive MV infection, as well as other neurotropic viral infections, may be due to induction of a unique profile of interferon-inducible genes. One of these genes, BST-2, inhibits release of enveloped viruses. Based on this observation, we investigated the ability of interferons and MV infection to induce BST-2 in primary neurons, and to explore the consequences of BST-2 expression on MV release. Despite low basal BST-2 expression in neurons as compared to primary fibroblasts and glial cells, Type I (IFNbeta) and Type II interferon (IFNgamma) exposure significantly induced BST-2 expression in neurons. MV-infection of neurons also elevated BST-2 levels, though interestingly, another enveloped RNA virus, lymphocytic choriomeningitis virus (LCMV), did not affect BST-2 levels, perhaps because of its capacity to block the host interferon response. This finding led us to investigate how MV induces BST-2. Utilizing neurons from Type I interferon receptor knockout (IFNAR KO) mice and STAT1 knockout mice, we found that MV upregulation of BST-2 is dependent on IFN production and signaling via STAT1, not viral replication itself. A cell line expressing tetracycline-inducible BST-2 was employed to show that extracellular MV is, in fact, limited by BST-2 expression.;Historically, interferons are known to inhibit viral spread and contain infection. Moreover, IFNgamma is recognized as a critical mediator of neurotropic MV infection. Although IFNgamma is crucial for non-cytolytic clearance of MV in vivo, the mechanisms by which it protects neurons from death and viral release are unknown. Type I interferons and IFNy were examined for their ability to limit viral RNA production and spread. Of note, Type I interferons and IFNgamma inhibited MV via different mechanisms: Type I interferons restricted extracellular MV release, while IFNgamma limited neuron-to-neuron spread. These findings will enable us to better understand the cell-specific responses to interferons induced by viral infection, and will elucidate how interferons function in the unique environment of the CNS.
机译：尽管神经元可以被麻疹病毒（MV）有效感染，但它们并没有表现出周围感染的两个主要特征：胞外病毒粒子的释放以及由于合胞体形成而引起的相关细胞病变。神经元如何在MV感染以及其他神经营养性病毒感染中生存，可能是由于诱导了干扰素诱导性基因的独特特征。这些基因之一BST-2可抑制包膜病毒的释放。基于此观察，我们调查了干扰素和MV感染在原代神经元中诱导BST-2的能力，并探讨了BST-2表达对MV释放的影响。尽管与初级成纤维细胞和神经胶质细胞相比，神经元中的基础BST-2表达较低，但暴露于I型（IFNbeta）和II型干扰素（IFNgamma）仍能明显诱导神经元中BST-2的表达。神经元的MV感染也升高了BST-2的水平，尽管有趣的是，另一种包膜RNA病毒，淋巴细胞脉络膜脑膜炎病毒（LCMV）并未影响BST-2的水平，这可能是因为它具有阻断宿主干扰素反应的能力。这一发现使我们研究了MV如何诱导BST-2。利用来自I型干扰素受体敲除（IFNAR KO）小鼠和STAT1敲除小鼠的神经元，我们发现BST-2的MV上调依赖于IFN的产生和通过STAT1的信号传导，而不是病毒复制本身。使用表达四环素诱导型BST-2的细胞系来证明细胞外MV实际上受BST-2表达的限制。历史上，已知干扰素可抑制病毒传播并包含感染。此外，IFNγ被认为是嗜神经性MV感染的关键介质。尽管IFNγ对于体内非溶细胞性清除至关重要，但它保护神经元免受死亡和病毒释放的机制尚不清楚。检查了I型干扰素和IFNγ限制病毒RNA产生和扩散的能力。值得注意的是，I型干扰素和IFNgamma通过不同机制抑制MV：I型干扰素限制细胞外MV释放，而IFNgamma限制神经元向神经元的扩散。这些发现将使我们能够更好地了解病毒感染诱导的干扰素的细胞特异性应答，并阐明干扰素在中枢神经系统独特环境中的功能。

著录项

  • 作者

    Holmgren, Alicia Marie.;

  • 作者单位

    Drexel University College of Medicine.;

  • 授予单位 Drexel University College of Medicine.;
  • 学科 Biology Microbiology.;Biology Virology.
  • 学位 Ph.D.
  • 年度 2013
  • 页码 113 p.
  • 总页数 113
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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