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Electrical activity and neuronal cell fusion in pseudorabies virus infection.

机译：伪狂犬病病毒感染中的电活动和神经元细胞融合。

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摘要

The pathologies of alphaherpesvirus infections tend to manifest as neuropathies of the peripheral nervous system: the tingle of an imminent cold sore, the neuralgia of shingles, or the "mad itch" of pseudorabies virus infection. In this thesis I report on studies concerning two phenomena related to these dysfunctions: cell fusion and electrical activity induced by pseudorabies virus (PRV) infection.;Investigation of cell fusion is motivated by seeking both a more thorough understanding of viral pathogenesis, and the capability of generating neuronal tracing viruses that do not so thoroughly disrupt the physiology of the cells they are used to study. I describe the current understanding of cell fusion induced by herpesviruses, and several approaches attempting to separate the propensity of PRV to induce cell fusion from its capacity to spread infection among neurons. All of the strains tested which were capable of spread also induced fusion. Notably, the cleavage of a particular protein (glycoprotein B) is ruled out as being required for induction of cell fusion.;The increased electrical activity in peripheral neurons infected by alphaherpesviruses is generally understood to be the proximate cause of peripheral neuropathies. I test the hypothesis that spread of infection is dependent upon this electrical activity, by testing the capacity of PRV to spread from neurons under different electrophysiological perturbations. Infected neurons are prevented from firing with a chemical neurotoxin, and induced to fire by both chemical methods and a novel application of optogenetics, which involves the use of light-gated ion channels to give precise control of excitation in neurons. These experiments reveal that electrical activity is not required for spread of infection, and further that increased activity can reduce the efficiency of spread. The results suggest that the electrical activity induced by PRV infection confers no benefits to viral survival or spread of infection at the cellular level.
机译：甲疱疹病毒感染的病理学往往表现为周围神经系统的神经病：即将来临的唇疱疹的刺痛，带状疱疹的神经痛或伪狂犬病病毒感染的“发痒”。在这篇论文中，我报告了有关与这些功能障碍有关的两种现象的研究：细胞融合和伪狂犬病病毒（PRV）感染引起的电活动。；对细胞融合的研究是通过寻求对病毒发病机理和功能的更全面了解而进行的产生的神经元示踪病毒没有彻底破坏它们用来研究的细胞的生理。我描述了当前对疱疹病毒诱导的细胞融合的理解，以及几种试图将PRV诱导细胞融合的倾向与其在神经元之间传播感染的能力分开的方法。所有能够传播的测试菌株也诱导融合。值得注意的是，排除了诱导蛋白质融合所必需的特定蛋白质（糖蛋白B）的裂解。被α疱疹病毒感染的周围神经元电活动的增强通常被认为是周围神经病的最直接原因。我通过测试PRV在不同电生理扰动下从神经元传播的能力来检验感染传播取决于这种电活动的假设。化学神经毒素可防止受感染的神经元激发，并通过化学方法和光遗传学的新应用诱导激发，这涉及光门控离子通道的使用，以精确控制神经元的激发。这些实验表明，电活动不是传播感染所必需的，而且活动的增加会降低传播的效率。结果表明，由PRV感染引起的电活动对病毒存活或感染在细胞水平的传播没有任何好处。

著录项

  • 作者

    Ambrosini, Anthony E.;

  • 作者单位

    Princeton University.;

  • 授予单位 Princeton University.;
  • 学科 Biology Virology.;Biology Neuroscience.;Biology Molecular.
  • 学位 Ph.D.
  • 年度 2014
  • 页码 124 p.
  • 总页数 124
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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