Immune Endocrine Epigenetics Research Group, Department of Infection and Immunity, Luxembourg Institute of Health, L-4345 Esch-sur-Alzette, Luxembourg.
Calbinotox, Faculty of Science and Technology, Lorraine University, 54506 Nancy, France.
Int J Mol Sci. 2020 Jul 19;21(14):5094. doi: 10.3390/ijms21145094.
A poor socioeconomic environment and social adversity are fundamental determinants of human life span, well-being and health. Previous influenza pandemics showed that socioeconomic factors may determine both disease detection rates and overall outcomes, and preliminary data from the ongoing coronavirus disease (COVID-19) pandemic suggests that this is still true. Over the past years it has become clear that early-life adversity (ELA) plays a critical role biasing the immune system towards a pro-inflammatory and senescent phenotype many years later. Cytotoxic T-lymphocytes (CTL) appear to be particularly sensitive to the early life social environment. As we understand more about the immune response to SARS-CoV-2 it appears that a functional CTL (CD8+) response is required to clear the infection and COVID-19 severity is increased as the CD8+ response becomes somehow diminished or exhausted. This raises the hypothesis that the ELA-induced pro-inflammatory and senescent phenotype may play a role in determining the clinical course of COVID-19, and the convergence of ELA-induced senescence and COVID-19 induced exhaustion represents the worst-case scenario with the least effective T-cell response. If the correct data is collected, it may be possible to separate the early life elements that have made people particularly vulnerable to COVID-19 many years later. This will, naturally, then help us identify those that are most at risk from developing the severest forms of COVID-19. In order to do this, we need to recognize socioeconomic and early-life factors as genuine medically and clinically relevant data that urgently need to be collected. Finally, many biological samples have been collected in the ongoing studies. The mechanisms linking the early life environment with a defined later-life phenotype are starting to be elucidated, and perhaps hold the key to understanding inequalities and differences in the severity of COVID-19.
贫穷的社会经济环境和社会逆境是人类寿命、幸福和健康的基本决定因素。以前的流感大流行表明,社会经济因素可能决定疾病的检出率和整体结果,而目前正在进行的冠状病毒病(COVID-19)大流行的初步数据表明,这仍然是正确的。过去几年,人们已经清楚地认识到,早期生活逆境(ELA)在多年后对免疫系统产生偏向促炎和衰老表型方面起着关键作用。细胞毒性 T 淋巴细胞(CTL)似乎对早期生活的社会环境特别敏感。随着我们对 SARS-CoV-2 的免疫反应的了解越来越多,似乎需要功能性 CTL(CD8+)反应来清除感染,而 COVID-19 的严重程度随着 CD8+反应的某种程度减弱或衰竭而增加。这就提出了一个假设,即 ELA 诱导的促炎和衰老表型可能在决定 COVID-19 的临床过程中发挥作用,ELA 诱导的衰老和 COVID-19 诱导的衰竭的收敛代表了最坏的情况,即 T 细胞反应最不有效。如果收集到正确的数据,就有可能将导致人们多年后特别容易感染 COVID-19 的早期生活因素分开。这自然会帮助我们识别出那些最有可能患上 COVID-19 最严重形式的人。为了做到这一点,我们需要认识到社会经济和早期生活因素是真正具有医学和临床相关性的数据,迫切需要收集这些数据。最后,在正在进行的研究中已经收集了许多生物样本。将早期生活环境与明确的后期生活表型联系起来的机制开始被阐明,这也许是理解 COVID-19 严重程度不平等和差异的关键。