Abstract：
Several traditional observational studies suggested an association between COVID-19 and leukocyte telomere length (LTL), a biomarker for biological age. However, whether there was a causal association between them remained unclear. We aimed to investigate whether genetically predicted COVID-19 is related to the risk of LTL, and vice versa. We performed bidirectional Mendelian randomization (MR) study using summary statistics from the genome-wide association studies of critically ill COVID-19 (n = 1 388 342) and LTL (n = 472 174) of European ancestry. The random-effects inverse-variance weighted estimation method was applied as the primary method with several other estimators as complementary methods. Using six single-nucleotide polymorphisms (SNPs) of genome-wide significance as instrumental variables for critically ill COVID-19, we did not find a significant association of COVID-19 on LTL (β = 0.0075, 95% confidence interval [CI]: -0.018 to 0.021, p = 0.733). Likewise, using 97 SNPs of genome-wide significance as instrumental variables for LTL, we did not find a significant association of LTL on COVID-19 (odds ratio = 1.00, 95% CI: 0.79-1.28, p = 0.973). Comparable results were obtained using MR-Egger regression, weighted median, and weighted mode approaches. We did not find evidence to support a causal association between COVID-19 and LTL in either direction.
摘要：
一些传统的观察性研究表明，COVID-19与白细胞端粒长度（LTL）之间存在关联，生物年龄的生物标志物。然而,两者之间是否存在因果关系尚不清楚.我们的目的是调查基因预测的COVID-19是否与LTL的风险有关，反之亦然。我们使用来自欧洲血统的重症COVID-19（n=1388342）和LTL（n=472174）的全基因组关联研究的汇总统计数据进行了双向孟德尔随机化（MR）研究。随机效应逆方差加权估计方法作为主要方法，其他几种估计方法作为补充方法。使用6个具有全基因组意义的单核苷酸多态性(SNP)作为重症COVID-19的辅助变量，我们没有发现COVID-19与LTL的显著关联(β=0.0075，95%置信区间[CI]:-0.018至0.021，p=0.733)。同样，使用97个具有全基因组意义的SNP作为LTL的工具变量，我们未发现LTL与COVID-19之间存在显著关联(比值比=1.00,95%CI:0.79-1.28,p=0.973).使用MR-Egger回归获得了可比的结果，加权中位数，和加权模式方法。我们没有发现证据支持COVID-19和LTL在任何方向上的因果关系。
