The Quebec
COVID-19
Biobank

Effective responses to the COVID-19 pandemic require novel solutions for research and responsible data sharing. Biobanking presents itself as a key priority in furthering our understanding of COVID-19. In this article, we propose a tripartite approach to consent to create resources for research relating to COVID-19. The approach aims to link three levels of participation: COVID-19 patients, respiratory/infectious disease patients, and longitudinal study participants. We explore the potential approaches that can be taken to consent processes with these three participant groups. We furthermore describe an access model for both single-site and multi-site data and sample storage. Through dealing with these topics at a high level, the model may be adapted to local legal and ethical requirements while still pursuing its ultimate goal: the creation of a research infrastructure that supports transparent, strong, and open science.

This two-sample Mendelian randomization study assessed whether genetically elevated 25-hydroxy vitamin D (25OHD) levels causally reduce COVID-19 susceptibility or severity. Using genetic instruments from a GWAS of 443,734 individuals and outcome data from the COVID-19 Host Genetics Initiative (up to 14,134 cases and 1.28 million controls), the analysis found no significant association between increased 25OHD levels and COVID-19 susceptibility (OR = 0.95), hospitalization (OR = 1.09), or severe disease (OR = 0.97). These findings were consistent across multiple analytic methods and sensitivity analyses. Results do not apply to individuals with vitamin D deficiency but suggest no causal protective role of vitamin D in the general population against COVID-19, calling into question the prioritization of vitamin D supplementation in COVID-19 prevention strategies.

To identify circulating proteins influencing Coronavirus Disease 2019 (COVID-19) susceptibility and severity, we undertook a two-sample Mendelian randomization (MR) study, rapidly scanning hundreds of circulating proteins while reducing bias due to reverse causation and confounding. In up to 14,134 cases and 1.2 million controls, we found that an s.d. increase in OAS1 levels was associated with reduced COVID-19 death or ventilation (odds ratio (OR) = 0.54, P = 7 × 10−8), hospitalization (OR = 0.61, P = 8 × 10−8) and susceptibility (OR = 0.78, P = 8 × 10−6). Measuring OAS1 levels in 504 individuals, we found that higher plasma OAS1 levels in a non-infectious state were associated with reduced COVID-19 susceptibility and severity. Further analyses suggested that a Neanderthal isoform of OAS1 in individuals of European ancestry affords this protection. Thus, evidence from MR and a case–control study support a protective role for OAS1 in COVID-19 adverse outcomes. Available pharmacological agents that increase OAS1 levels could be prioritized for drug development.