Laboratory of Electron Microscopy, National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Rome, Italy.
Laboratory of Virology, National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Rome, Italy.
Cell Death Dis. 2021 Mar 12;12(3):263. doi: 10.1038/s41419-021-03527-9.
The pathogenesis of SARS-CoV-2 remains to be completely understood, and detailed SARS-CoV-2 cellular cytopathic effects requires definition. We performed a comparative ultrastructural study of SARS-CoV-1 and SARS-CoV-2 infection in Vero E6 cells and in lungs from deceased COVID-19 patients. SARS-CoV-2 induces rapid death associated with profound ultrastructural changes in Vero cells. Type II pneumocytes in lung tissue showed prominent altered features with numerous vacuoles and swollen mitochondria with presence of abundant lipid droplets. The accumulation of lipids was the most striking finding we observed in SARS-CoV-2 infected cells, both in vitro and in the lungs of patients, suggesting that lipids can be involved in SARS-CoV-2 pathogenesis. Considering that in most cases, COVID-19 patients show alteration of blood cholesterol and lipoprotein homeostasis, our findings highlight a peculiar important topic that can suggest new approaches for pharmacological treatment to contrast the pathogenicity of SARS-CoV-2.
SARS-CoV-2 的发病机制仍未完全阐明，需要详细定义 SARS-CoV-2 的细胞致病作用。我们对 SARS-CoV-1 和 SARS-CoV-2 在 Vero E6 细胞和死于 COVID-19 的患者肺组织中的感染进行了比较超微结构研究。SARS-CoV-2 诱导快速死亡，与 Vero 细胞的深刻超微结构变化相关。肺组织中的 II 型肺泡细胞表现出明显的改变特征，有空泡和肿胀的线粒体，存在丰富的脂滴。脂类的积累是我们在 SARS-CoV-2 感染的细胞中观察到的最显著的发现，无论是在体外还是在患者的肺组织中，这表明脂类可能参与了 SARS-CoV-2 的发病机制。鉴于在大多数情况下，COVID-19 患者的血液胆固醇和脂蛋白稳态发生改变，我们的研究结果强调了一个特别重要的问题，这可能提示新的药物治疗方法来对抗 SARS-CoV-2 的致病性。
