OBJECTIVE
To investigate the relationship between depressive symptoms and risk for COVID-19 hospitalization and death in a United States general population-based sample.
METHODS
We studied participants enrolled into observational NIH-funded cohorts from 1971-2010 with ongoing follow-up through 2023. Pre-pandemic Centers for Epidemiologic Studies Depression (CES-D) 10-item scale scores ≥10 defined elevated depressive symptoms. Questionnaires, medical records, and death certificates classified incident COVID-19 as severe (hospitalized/fatal) or non-severe from April 2020 through February 2023.
RESULTS
Of 33,565 participants, 633 (1.9%) had incident severe COVID-19 over a mean (SD) follow-up of 453 (207) days. Elevated pre-pandemic depressive symptoms were present in 4,922 (16.3%) of participants. Elevated pre-pandemic depressive symptoms increased the hazard of severe COVID-19 in fully-adjusted (aHR=1.27; 95%CI: 1.03-1.57) models. In sex-stratified models (p-interaction=0.03), elevated depressive symptoms increased the hazard in women (aHR=1.49; 95%CI: 1.17-1.90) but not in men (aHR=0.96; 95%CI: 0.67-1.39).
CONCLUSIONS
Pre-pandemic depressive symptoms were associated with increased risk of severe COVID-19 among women in a large US general population-based study of adults, and associations in men were neither confirmed nor ruled out. These results support current CDC recommendations that depression be considered an underlying medical condition associated with higher risk for severe COVID-19 and suggest that increased clinical focus on risk mitigation for COVID-19 and other acute respiratory infections among patients with depressive symptoms is warranted.
E. Oelsner, Yi-Fei Sun, P. Balte et al.· Biopsychosocial science and...· 0 citations
Interleukin 33 (IL-33) is a cytokine of the IL-1 family that acts as an alarmin in both innate and adaptive immunity. IL-33 is constitutively nuclear in epithelial and endothelial cells, where its activity is limited by nuclear retention. Release of IL-33 in response to cellular stress or injury can mediate type 2 immune responses or tissue repair, depending on the local tissue environment. IL-33 activity is regulated at multiple levels, including nuclear retention, oxidation, proteolytic processing, and metabolic regulation. Following its release, oxidation rapidly suppresses IL-33 activity, while mast cell and neutrophil proteases can generate smaller active fragments that target cells expressing the IL-33 ST2 receptor. Simultaneously, tissue metabolic status influences cellular responsiveness through the mTORC1 and AMPK pathways, which link metabolic capacity to effector function. These conditions may explain why IL-33 can mediate an inflammatory response, but in other circumstances, it contributes to tissue repair. Such pleiotropic properties may also underline the variability in clinical responses to IL-33/ST2-targeted therapies across various diseases. The appreciation of IL-33 as a cytokine whose activity is conditioned by its structural, redox, and metabolic environment is critical to optimizing its therapeutic potential as a target.
Fernanda Martinez-Moreno, E. Jerschow, Victor E. Ortega et al.· Frontiers in Allergy· 0 citations
Most genetic variants associated with complex traits are hypothesized to regulate gene expression. To understand the genetics underlying gene expression variability, we characterized 14,324 RNA-sequencing samples from the Trans-Omics for Precision Medicine program and performed expression and splicing quantitative trait locus (e/sQTL) analyses in six tissues and cell types, including whole blood (n = 6454) and lung (n = 1291). We detected tens of thousands of secondary cis-e/sQTLs, showing that secondary cis-e/sQTL discovery remains unsaturated. We fine-mapped UK Biobank-derived genome-wide association study (GWAS) signals from 164 traits and identified e/sQTL colocalizations for 10,611 GWAS signals, including 7096 that colocalize with secondary e/sQTLs. Our results suggest that even larger e/sQTL analyses will uncover additional secondary e/sQTLs, further benefiting GWAS interpretation.
Peter Orchard, T. Blackwell, L. Kachuri et al.· Science· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
