Clinical, regional, and genetic characteristics of Covid-19 patients from UK Biobank

Abstract

Background Coronavirus disease 2019 (Covid-19) has rapidly infected millions of people worldwide. Recent studies suggest that racial minorities and patients with comorbidities are at higher risk of Covid-19. In this study, we analyzed the effects of clinical, regional, and genetic factors on Covid-19 positive status. Methods The UK Biobank is a longitudinal cohort study that recruited participants from 2006 to 2010 from throughout the United Kingdom. Covid-19 test results were provided to UK Biobank starting on March 16, 2020. The main outcome measure in this study was Covid-19 positive status, determined by the presence of any positive test for a single individual. Clinical risk factors were derived from UK Biobank at baseline, and regional risk factors were imputed using census features local to each participant’s home zone. We used robust adjusted Poisson regression with clustering by testing laboratory to estimate relative risk. Blood types were derived using genetic variants rs8176719 and rs8176746, and genomewide tests of association were conducted using logistic-Firth hybrid regression. Results This prospective cohort study included 397,064 UK Biobank participants, of whom 968 tested positive for Covid-19. The unadjusted relative risk of Covid-19 for Black participants was 3.66 (95% CI 2.83–4.74), compared to White participants. Adjusting for Townsend deprivation index alone reduced the relative risk to 2.44 (95% CI 1.86–3.20). Comorbidities that significantly increased Covid-19 risk included chronic obstructive pulmonary disease (adjusted relative risk [ARR] 1.64, 95% CI 1.18–2.27), ischemic heart disease (ARR 1.48, 95% CI 1.16–1.89), and depression (ARR 1.32, 95% CI 1.03–1.70). There was some evidence that angiotensin converting enzyme inhibitors (ARR 1.48, 95% CI 1.13–1.93) were associated with increased risk of Covid-19. Each standard deviation increase in the number of total individuals living in a participant’s locality was associated with increased risk of Covid-19 (ARR 1.14, 95% CI 1.08–1.20). Analyses of genetically inferred blood types confirmed that participants with type A blood had increased odds of Covid-19 compared to participants with type O blood (odds ratio [OR] 1.16, 95% CI 1.01–1.33). A meta-analysis of genomewide association studies across ancestry groups did not reveal any significant loci. Study limitations include confounding by indication, bias due to limited information on early Covid-19 test results, and inability to accurately gauge disease severity. Conclusions When assessing the association of Black race with Covid-19, adjusting for deprivation reduced the relative risk of Covid-19 by 33%. In the context of sociological research, these findings suggest that discrimination in the labor market may play a role in the high relative risk of Covid-19 for Black individuals. In this study, we also confirmed the association of blood type A with Covid-19, among other clinical and regional factors.

Changes in Smoking Behaviour and Home-Smoking Rules during the Initial COVID-19 Lockdown Period in Israel

“…Currently, there is uncertainty regarding the association between smoking and SARS-CoV-2 infection and severity [ 17 ]. Several studies have reported that current smokers have lower than expected risk for SARS-CoV-2 infection, [ 18 , 19 , 20 , 21 , 22 ] while other studies have suggested that hospitalized smokers with SARS-CoV-2 infection have an increased risk for a severe infection [ 3 , 23 ].…”

Coronavirus infection: An immunologists' perspective

“…Its content in the lung increases upon inflammation and inflammatory cytokines, and consequently, lung levels of C3 are increased in patients with lung diseases 87 . As expected, SARS‐CoV‐2‐infected patients with lung illness have a higher risk to progress to severe disease and die 88 . Since C3 is involved in airway disease and emphysema, 89 COPD patients with high levels of C3 and infected with SARS‐CoV‐2 may be more susceptible to develop a severe disease that stable COPD patients without exacerbations and treated with anti‐inflammatory therapy 90 …”

“…87 As expected, SARS-CoV-2-infected patients with lung illness have a higher risk to progress to severe disease and die. 88 Since C3 is involved in airway disease and emphysema, 89 COPD patients with high levels of C3 and infected with SARS-CoV-2 may be more susceptible to develop a severe disease that stable COPD patients without exacerbations and treated with anti-inflammatory therapy. 90 Polycarpou et al 91 have an exciting approach to managing complement and the deleterious effect of the innate immune response in COVID-19 patients.…”

Association of Sickle Cell Trait with Risk and Mortality of COVID-19: Results from the United Kingdom Biobank

“…Most of these findings are consistent with those of other published studies. 2,3 Compared with individuals who were not SCT carriers, SCT carriers had similar COVID-19 positivity rates but higher COVID-19 mortality rates overall among Black individuals (Table 1). For Black individuals, the positivity rates were 19.7% (14/71) and 21.1% (167/791) for subjects with SCT and without SCT (P 5 0.96).…”

“…1 This finding is supported by United Kingdom Biobank (UKB) studies, which found significantly higher positive rates among Black individuals even after adjusting for biological, behavioral, and socioeconomic factors. 2,3 Additionally, evidence shows that individuals with chronic conditions such as cardiovascular disease, diabetes, chronic respiratory disease, hypertension, and sickle cell disease (SCD) are particularly vulnerable to more severe COVID-19 disease. 1,4 The intersection of race and SCD makes it important to consider their impact on COVID-19.…”