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Shorter telomere lengths in patients with severe COVID-19 disease

机译:严重的Covid-19疾病患者的较短端粒长度

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摘要

The incidence of severe manifestations of COVID-19 increases with age with older patients showing the highest mortality, suggesting that molecular pathways underlying aging contribute to the severity of COVID-19. One mechanism of aging is the progressive shortening of telomeres, which are protective structures at chromosome ends. Critically short telomeres impair the regenerative capacity of tissues and trigger loss of tissue homeostasis and disease. The SARS-CoV-2 virus infects many different cell types, forcing cell turn-over and regeneration to maintain tissue homeostasis. We hypothesize that presence of short telomeres in older patients limits the tissue response to SARS-CoV-2 infection. We measure telomere length in peripheral blood lymphocytes COVID-19 patients with ages between 29 and 85 years-old. We find that shorter telomeres are associated to increased severity of the disease. Individuals within the lower percentiles of telomere length and higher percentiles of short telomeres have higher risk of developing severe COVID-19 pathologies.
机译:Covid-19严重表现的发生率随着年龄的增长而增加,具有较高的死亡率,表明衰老的分子途径有助于Covid-19的严重程度。一种老化机制是端粒的逐步缩短,其是染色体末端的保护结构。批判性短端粒损害组织的再生能力,并引发组织稳态和疾病的丧失。 SARS-COV-2病毒感染了许多不同的细胞类型,强迫细胞翻转和再生以维持组织稳态。我们假设老年患者的短端粒体存在限制组织对SARS-COV-2感染的影响。我们测量外周血淋巴细胞Covid-19患者29至85岁的患者的端粒长度。我们发现较短的端粒与增加的疾病严重程度有关。较低百分位数的端粒长度百分位数和较高百分位的短端粒百分比具有更高的发展严重Covid-19病理的风险。

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