Verevka S V
Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv.
Ukr Biokhim Zh (1999). 2003 Jan-Feb;75(1):115-20.
Declining of unproved supposition about the transformation of the cellular isoform of prion protein into pathogenic one allows the pathogenesis of prion diseases to be reduced to the series of interdependent processes caused by prion-mediated selective damage of the components of the cell chaperoning system with following membrane folding of the de novo synthesized prion protein. Dependence of the level of the cell chaperoning system damage on the similarity of the sequences of cellular and infectious prion proteins explains exhaustively the existence of interspecies barrier in prion pathogenesis as well as makes it natural and inevitable property of the latter. The structural ensurance of separate prion diseases strains, their transformation at repeated infectious passages commonly with known and supposed ways for prion-less initiation of spongiform encephalopathies are discussed.
关于朊病毒蛋白细胞异构体向致病异构体转化的未经证实的假设的衰落,使得朊病毒疾病的发病机制归结为由朊病毒介导的细胞伴侣系统成分的选择性损伤以及随后新生合成的朊病毒蛋白的膜折叠所引起的一系列相互依存的过程。细胞伴侣系统损伤水平对细胞型和感染性朊病毒蛋白序列相似性的依赖性,详尽地解释了朊病毒发病机制中种间屏障的存在,并使其成为后者自然且不可避免的特性。本文还讨论了不同朊病毒疾病毒株的结构保证,以及它们在重复感染传代过程中的转化,通常采用已知的和推测的无朊病毒引发海绵状脑病的方式。