St. Petersburg Branch, Vavilov Institute of General Genetics, St. Petersburg, Russian Federation.
Department of Genetics and Biotechnology, St. Petersburg State University, St. Petersburg, Russian Federation.
Prion. 2021 Dec;15(1):53-55. doi: 10.1080/19336896.2021.1910468.
The severe course of COVID-19 causes systemic chronic inflammation and thrombosis in a wide variety of organs and tissues. The nature of these inflammations remains a mystery, although they are known to occur against the background of a high level of cytokine production. The high level of cytokines provokes overproduction of the Serum amyloid A (SAA) protein. Moreover, the number of studies has shown that the severe COVID-19 causes SAA overproduction. The authors of these works regard a high level of SAA exclusively as a biomarker of COVID-19. However, it should be borne in mind that overproduction of SAA can cause systemic AA amyloidosis. SAA forms cytotoxic amyloid deposits in various organs and induces inflammation and thrombosis. The consequences of COVID-19 infection are surprisingly similar to the clinical picture that is observed in AA amyloidosis. Here I present the hypothesis that AA amyloidosis is a factor causing systemic complications after coronavirus disease.
COVID-19 的严重病程会在多种器官和组织中引起全身性慢性炎症和血栓形成。尽管已知这些炎症是在细胞因子产生水平高的背景下发生的,但它们的性质仍不清楚。细胞因子水平升高会促使血清淀粉样蛋白 A(SAA)蛋白过度产生。此外,大量研究表明,严重的 COVID-19 会导致 SAA 过度产生。这些研究的作者将高水平的 SAA 仅视为 COVID-19 的生物标志物。然而,应该记住的是,SAA 的过度产生会导致全身性 AA 淀粉样变性。SAA 在各种器官中形成细胞毒性淀粉样沉积物,并引发炎症和血栓形成。COVID-19 感染的后果与 AA 淀粉样变性中观察到的临床特征惊人地相似。在这里,我提出假说,即 AA 淀粉样变性是冠状病毒病后全身并发症的一个致病因素。