Chinese Institute for Brain Research, Beijing 102206, China.
Viruses. 2022 Aug 31;14(9):1940. doi: 10.3390/v14091940.
Generating a prion with exogenously produced recombinant prion protein is widely accepted as the ultimate proof of the prion hypothesis. Over the years, a plethora of misfolded recPrP conformers have been generated, but despite their seeding capability, many of them have failed to elicit a fatal neurodegenerative disorder in wild-type animals like a naturally occurring prion. The application of the protein misfolding cyclic amplification technique and the inclusion of non-protein cofactors in the reaction mixture have led to the generation of authentic recombinant prions that fully recapitulate the characteristics of native prions. Together, these studies reveal that recPrP can stably exist in a variety of misfolded conformations and when inoculated into wild-type animals, misfolded recPrP conformers cause a wide range of outcomes, from being completely innocuous to lethal. Since all these recPrP conformers possess seeding capabilities, these results clearly suggest that seeding activity alone is not equivalent to prion activity. Instead, authentic prions are those PrP conformers that are not only heritable (the ability to seed the conversion of normal PrP) but also pathogenic (the ability to cause fatal neurodegeneration). The knowledge gained from the studies of the recombinant prion is important for us to understand the pathogenesis of prion disease and the roles of misfolded proteins in other neurodegenerative disorders.
用外源产生的重组朊病毒蛋白产生朊病毒被广泛认为是朊病毒假说的最终证据。多年来,已经产生了大量错误折叠的 recPrP 构象,但尽管它们具有引发能力,但其中许多构象未能在野生型动物中引发致命的神经退行性疾病,就像天然存在的朊病毒一样。蛋白质错误折叠循环扩增技术的应用以及在反应混合物中包含非蛋白质辅助因子,导致产生了完全重现天然朊病毒特征的真正重组朊病毒。这些研究共同表明,recPrP 可以稳定存在于多种错误折叠构象中,并且当接种到野生型动物中时,错误折叠的 recPrP 构象会导致从完全无害到致命的广泛结果。由于所有这些 recPrP 构象都具有引发能力,这些结果清楚地表明,引发活性本身不等同于朊病毒活性。相反,真正的朊病毒是那些不仅具有遗传性(引发正常 PrP 转化的能力)而且具有致病性(引起致命神经退行性变的能力)的 PrP 构象。从重组朊病毒研究中获得的知识对于我们理解朊病毒病的发病机制以及错误折叠蛋白质在其他神经退行性疾病中的作用非常重要。