Pérez-Torres Israel, Guarner-Lans Verónica, Soria-Castro Elizabeth, Manzano-Pech Linaloe, Palacios-Chavarría Adrián, Valdez-Vázquez Rafael Ricardo, Domínguez-Cherit Jose Guillermo, Herrera-Bello Hector, Castillejos-Suastegui Humberto, Moreno-Castañeda Lidia, Alanís-Estrada Gabriela, Hernández Fabián, González-Marcos Omar, Márquez-Velasco Ricardo, Soto María Elena
Departament of Cardiovascular Biomedicine, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Departament of Physiology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Front Physiol. 2021 May 11;12:667024. doi: 10.3389/fphys.2021.667024. eCollection 2021.
The kidnapping of the lipid metabolism of the host's cells by severe acute respiratory syndrome (SARS-CoV-2) allows the virus to transform the cells into optimal machines for its assembly and replication. Here we evaluated changes in the fatty acid (FA) profile and the participation of the activity of the desaturases, in plasma of patients with severe pneumonia by SARS-CoV-2. We found that SARS-CoV-2 alters the FA metabolism in the cells of the host. Changes are characterized by variations in the desaturases that lead to a decrease in total fatty acid (TFA), phospholipids (PL) and non-esterified fatty acids (NEFAs). These alterations include a decrease in palmitic and stearic acids ( ≤ 0.009) which could be used for the formation of the viral membranes and for the reparation of the host's own membrane. There is also an increase in oleic acid (OA; = 0.001) which could modulate the inflammatory process, the cytokine release, apoptosis, necrosis, oxidative stress (OS). An increase in linoleic acid (LA) in TFA ( = 0.03) and a decreased in PL ( = 0.001) was also present. They result from damage of the internal mitochondrial membrane. The arachidonic acid (AA) percentage was elevated ( = 0.02) in the TFA and this can be participated in the inflammatory process. EPA was decreased ( = 0.001) and this may decrease of pro-resolving mediators with increase in the inflammatory process. The total of NEFAs ( = 0.03), PL ( = 0.001), cholesterol, HDL and LDL were decreased, and triglycerides were increased in plasma of the COVID-19 patients. Therefore, SARS-CoV-2 alters the FA metabolism, the changes are characterized by alterations in the desaturases that lead to variations in the TFA, PL, and NEFAs profiles. These changes may favor the replication of the virus but, at the same time, they are part of the defense system provided by the host cell metabolism in its eagerness to repair damage caused by the virus to cell membranes.
严重急性呼吸综合征冠状病毒2(SARS-CoV-2)劫持宿主细胞的脂质代谢,使病毒能够将细胞转变为用于其组装和复制的最佳机器。在此,我们评估了SARS-CoV-2所致重症肺炎患者血浆中脂肪酸(FA)谱的变化以及去饱和酶活性的参与情况。我们发现,SARS-CoV-2改变了宿主细胞中的FA代谢。变化的特征在于去饱和酶的变化,这导致总脂肪酸(TFA)、磷脂(PL)和非酯化脂肪酸(NEFA)减少。这些改变包括棕榈酸和硬脂酸减少(≤0.009),它们可用于形成病毒膜以及修复宿主自身的膜。油酸(OA;=0.001)也增加,其可调节炎症过程、细胞因子释放、凋亡、坏死、氧化应激(OS)。TFA中亚油酸(LA)增加(=0.03)且PL减少(=0.001)。它们是线粒体内膜损伤的结果。TFA中花生四烯酸(AA)百分比升高(=0.02),这可参与炎症过程。二十碳五烯酸(EPA)减少(=0.001),这可能随着炎症过程的增加而减少促消退介质。COVID-19患者血浆中NEFAs总量(=0.03)、PL(=0.001)、胆固醇、高密度脂蛋白和低密度脂蛋白减少,甘油三酯增加。因此,SARS-CoV-2改变了FA代谢,其变化的特征是去饱和酶的改变,导致TFA、PL和NEFAs谱发生变化。这些变化可能有利于病毒的复制,但同时,它们也是宿主细胞代谢在急于修复病毒对细胞膜造成的损伤时所提供的防御系统的一部分。