Speaker: Dr. Wonil Chung Place: Online via Zoom, Zoom ID: 938 0290 9321 / Passcode: ams Time:
About the speaker
Dr. Wonil Chung is an Assistant Professor in Statistics at Soongsil University. Before that, he was a research associate at Harvard T.H. Chan School of Public Health and received his Ph.D. degree in Biostatistics from the University of North Carolina at Chapel Hill (UNC) and MS and BS degrees in Statistics from Seoul National University. His research interests are in Biostatistics, Statistical Genetics, Big Data, Statistical Learning and Deep Learning.
Although Type 2 diabetes (T2D) have been known as one of the important risk factors for the severity and mortality of COVID-19, the effect of T2D and its genetic susceptibility on COVID-19 are largely unknown. We analyzed the population-based cohort data of 459,188 individuals from UK Biobank with COVID-19 test results, individuals’ hospitalization data and death-related records during the period from March 11, 2020 to December 20, 2021. First, we investigated the association of T2D, and its genetic susceptibility with COVID-19 infection using multivariable logistic regression model. To capture overall genetic susceptibility for T2D, we computed polygenic risk scores (PRS) based on summary statistics from UK Biobank. In the multivariable logistic models, we found that the odds ratio (OR) of T2D was 1.555 (P= 3.49*10-86) and OR of PRS for T2D with one-unit (=standard deviation) increase in PRS was 1.064 (P=3.11*10-12), indicating the roles of T2D-related genetics in the pathogenesis of COVID-19 infection. Next, we performed multivariable Cox proportional hazard models to investigate the effect of T2D patients infected with COVID-19 on the survival times. The estimated survival curves and pairwise log-rank tests showed that the estimated hazard for COVID-19 infected T2D patients were 4.67 times (P=9.88*10-324) and 2.58 times (P=6.20*10-231) higher than individuals without COVID-19 infection and T2D, respectively and the hazard ratio (HR) of PRS for T2D with one-unit increase in PRS was 1.088 (P=4.76*10-14). Furthermore, we found the mortality of COVID-19 infected T2D patients was dramatically increased compared to T2D patients not infected with COVID-19 and the mortality of individuals with high genetic susceptibility for T2D was increased as well.