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首页> 外文期刊>The FEBS journal >The reconstitution of mammalian prion infectivity de novo
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The reconstitution of mammalian prion infectivity de novo

机译：从头开始重新构建哺乳动物病毒感染力

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The discovery of prion disease transmission in mammals, as well as a non-Mendelian type of inheritance in yeast, has led to the establishment of a new concept in biology, the prion hypothesis. The prion hypothesis postulates that an abnormal protein conformation propagates itself in an autocatalytic manner using the normal isoform of the same protein as a substrate and thereby acts either as a transmissible agent of disease (in mammals), or as a heritable determinant of phenotype (in yeast and fungus). While the prion biology of yeast and fungus supports this idea strongly, the direct proof of the prion hypothesis in mammals, specifically the reconstitution of the disease-associated isoform of the prion protein (PrPSc) in vitro de novo from noninfectious prion protein, has been difficult to achieve despite many years of effort. The present review summarizes our current knowledge about the biochemical nature of the prion infectious agent and structure of PrPSc, describes potential strategies for generating prion infectivity de novo and provides some insight on why the reconstitution of infectivity has been difficult to achieve in vitro. Several hypotheses are proposed to explain the apparently low infectivity of the first generation of recently reported synthetic mammalian prions.
机译：在哺乳动物中disease病毒疾病传播的发现以及酵母中非孟德尔遗传的发现，导致了生物学上新概念的建立，即ion病毒假说。病毒假说假设异常蛋白质构象以相同蛋白质的正常同工型作为底物以自身催化方式自我传播，从而充当疾病的可传播因子（在哺乳动物中）或作为表型的遗传决定因素（在酵母和真菌）。尽管酵母和真菌的病毒生物学强有力地支持了这一观点，但哺乳动物中the病毒假说的直接证据，特别是在体外从无感染性ion病毒蛋白中重新构建了与疾病相关的pr病毒蛋白同工型（PrPSc）。尽管经过多年的努力，还是很难实现。本综述总结了我们目前关于about病毒感染剂的生化性质和PrPSc结构的知识，描述了从头产生generating病毒感染性的潜在策略，并对为何难以在体外实现感染性重构提供了一些见识。提出了几种假设来解释最近报道的合成哺乳动物病毒的第一代的明显低感染性。

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