Faculty of Medicine, School of Translational Health Science, Southmead Hospital, University of Bristol, Bristol, United Kingdom.
Front Endocrinol (Lausanne). 2020 Sep 17;11:582870. doi: 10.3389/fendo.2020.582870. eCollection 2020.
The pandemic of COVID-19, caused by the coronavirus, SARS-CoV-2, has had a global impact not seen for an infectious disease for over a century. This acute pandemic has spread from the East and has been overlaid onto a slow pandemic of metabolic diseases of obesity and diabetes consequent from the increasing adoption of a Western-lifestyle characterized by excess calorie consumption with limited physical activity. It has become clear that these conditions predispose individuals to a more severe COVID-19 with increased morbidity and mortality. There are many features of diabetes and obesity that may accentuate the clinical response to SARS-CoV-2 infection: including an impaired immune response, an atherothrombotic state, accumulation of advanced glycation end products and a chronic inflammatory state. These could prime an exaggerated cytokine response to viral infection, predisposing to the cytokine storm that triggers progression to septic shock, acute respiratory distress syndrome, and multi-organ failure. Infection leads to an inflammatory response and tissue damage resulting in increased metabolic activity and an associated increase in the mechanisms by which cells ingest and degrade tissue debris and foreign materials. It is becoming clear that viruses have acquired an ability to exploit these mechanisms to invade cells and facilitate their own life-cycle. In obesity and diabetes these mechanisms are chronically activated due to the deteriorating metabolic state and this may provide an increased opportunity for a more profound and sustained viral infection.
由冠状病毒 SARS-CoV-2 引起的 COVID-19 大流行是一个多世纪以来未曾见过的全球性传染病。这种急性大流行从东部开始蔓延,并叠加在肥胖和糖尿病等代谢性疾病的慢性大流行之上,这些疾病是由于越来越多地采用西方生活方式导致的,其特点是过量卡路里摄入和有限的体力活动。很明显,这些情况使个体更容易出现更严重的 COVID-19,导致发病率和死亡率增加。糖尿病和肥胖症有许多特征可能会加重对 SARS-CoV-2 感染的临床反应:包括免疫反应受损、动脉粥样硬化状态、晚期糖基化终产物的积累和慢性炎症状态。这些可能会引发对病毒感染的过度细胞因子反应,从而导致细胞因子风暴,引发脓毒性休克、急性呼吸窘迫综合征和多器官衰竭。感染会导致炎症反应和组织损伤,从而导致代谢活动增加,并与细胞摄取和降解组织碎片和外来物质的机制相关联。越来越明显的是,病毒已经获得了利用这些机制入侵细胞并促进自身生命周期的能力。在肥胖和糖尿病中,由于代谢状态恶化,这些机制会持续激活,这可能为更严重和持续的病毒感染提供更多机会。