Near the end of 2019, SARS-CoV-2, a novel highly contagious coronavirus phylogenetically related to the SARS virus, entered the human population with lethal consequences. This special issue devoted to the resulting disease COVID-19 was not planned but instead the articles accumulated organically as researchers in the cell stress response field noticed similarities among the pathophysiology of COVID-19 infections and the responses that they studied in contexts unrelated to viral infection. We preface the issue with an introductory article which begins with a brief review of the structure and biology of SARS-CoV-2. As we collected and compared the COVID-19 articles, several shared themes emerged. In the second part of the introduction, each article is summarized briefly and the common themes that link each into a spontaneously arising chain of ideas and hypotheses are emphasized. These themes include growing evidence of molecular mimicry among the viral proteins and the proteins of patients. The realization that much of the consequences of such immune mimicry may play out on the plasma membrane of vascular endothelial cells raised the specter of autoimmune-induced vascular endothelial damage in multiple organs. Proposals of new therapeutic approaches have coalesced around the theme of inducing protection of the vascular endothelium. New chemical treatments that are proposed include stannous chloride, inducers of the gasotransmitter hydrogen sulfide such as sodium thiosulfate and inducers of the cytoprotective stress protein heme oxygenase. Oxygen delivered by ventilators is already in extensive use to provide life support for patients with severe COVID-19. Two articles propose to advance the use of oxygen to the level of a therapeutic treatment early in the detection of the virus in infected patients by delivering oxygen under elevated pressure in hyperbaric chambers. At elevated blood plasma concentrations, hyperbaric oxygen is capable of achieving results far beyond the capability of ventilators as it promotes the activation of transcription factors that control the establishment of inducible cellular defense systems.

中文翻译：

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冠状病毒和压力：从细胞到全球。

到2019年底，SARS-CoV-2是一种与SARS病毒发生系统相关的新型高度传染性冠状病毒，它对人类造成了致命的后果。这个专门针对导致疾病COVID-19的特刊没有计划，但随着细胞应激反应领域的研究人员注意到COVID-19感染的病理生理学和他们在与病毒感染无关的背景下研究的反应之间的相似性，文章有机地积累了起来。 。我们以介绍性文章作为开头，首先简要回顾一下SARS-CoV-2的结构和生物学。当我们收集和比较COVID-19文章时，出现了几个共享的主题。在引言的第二部分，每篇文章都进行了简要总结，并强调了将各自链接到自发产生的思想和假设链的共同主题。这些主题包括病毒蛋白和患者蛋白之间分子模仿的越来越多的证据。这种免疫模拟的许多后果可能会在血管内皮细胞的质膜上发挥作用的认识提高了自身免疫性引起的多个器官血管内皮损伤的可能性。关于诱导血管内皮保护的主题，新的治疗方法的提案已经合并。提出了新的化学处理方法，包括氯化亚锡，气体传递硫化氢的诱导剂（如硫代硫酸钠）和细胞保护性应激蛋白血红素加氧酶的诱导剂。呼吸机输送的氧气已经广泛用于为重症COVID-19的患者提供生命支持。有两篇文章提出，通过在高压室中在高压下输送氧气，将氧气的使用率提高到感染患者检测病毒早期的治疗水平。在升高的血浆浓度下，高压氧能够实现远远超出呼吸机能力的结果，因为它促进了控制诱导型细胞防御系统建立的转录因子的激活。有两篇文章提出，通过在高压室中在高压下输送氧气，将氧气的使用提高到感染患者检测病毒早期的治疗水平。在升高的血浆浓度下，高压氧能够实现远远超出呼吸机能力的结果，因为它促进了控制诱导型细胞防御系统建立的转录因子的激活。有两篇文章提出，通过在高压室中在高压下输送氧气，将氧气的使用提高到感染患者检测病毒早期的治疗水平。在升高的血浆浓度下，高压氧能够实现远远超出呼吸机能力的结果，因为它促进了控制诱导型细胞防御系统建立的转录因子的激活。