Association of blood type A with increased risk of severe COVID-19 in healthcare workers.
Ontology highlight
ABSTRACT:
SUBMITTER: Mahajan NN
PROVIDER: S-EPMC8380301 | biostudies-literature |
REPOSITORIES: biostudies-literature
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2020-07-06 | GSE149689 | GEO
Project description:Early in the COVID-19 pandemic, type 2 diabetes (T2D) was marked as a risk-factor for severe disease. Inflammation is central to the aetiology of both conditions where immune responses influence disease course. Identifying at-risk groups through immuno-inflammatory signatures can direct personalised care and help develop potential targets for precision therapy. This observational study characterised immunophenotypic variation associated with COVID-19 severity in T2D. Broad-spectrum immunophenotyping quantified 15 leukocyte populations in circulation from a cohort of 45 hospitalised COVID-19 patients with and without T2D. Lymphocytopenia, of CD8+ lymphocytes, was associated with severe COVID-19 and intensive care admission in non-diabetic and T2D patients. A morphological anomaly of increased monocyte size and monocytopenia of classical monocytes were specifically associated with severe COVID-19 in patients with T2D requiring intensive care. Over-expression of inflammatory markers reminiscent of the type-1 interferon pathway underlaid the immunophenotype associated with T2D. These changes may contribute to severity of COVID-19 in T2D. These findings show characteristics of severe COVID-19 in T2D as well as provide evidence that type-1 interferons may be actionable targets for future studies.
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Project description:Recent data has revealed an association between coronavirus disease-19 (COVID-19) incidence and seasonally regulated androgen sensitivity. This potential relationship between SARS-CoV-2 infection and clock genes, coupled with previously reported effects of night shift work on health, leads us to hypothesize that night shift workers may be at an increased physiological risk of coronavirus disease-19 (COVID-19). Shift work, especially night shift work, has long been associated with several chronic health conditions. The mechanisms that drive these associations are not well understood; however, current literature suggests that the disruption of circadian rhythms may cause downstream hormonal and immune effects that render night shift workers more susceptible to disease. First, circadian rhythms may play a role in the mechanism of viral infection, as viral vaccines administered in the morning elicit greater immune responses than those administered in the afternoon. Next, increased exposure to light at night may inhibit the production of melatonin, which has been observed to enhance DNA repair and shown to upregulate expression of Bmal1, an established inhibitor of herpes simplex virus and influenza. Finally, abnormal immune cell and cytokine levels have been observed following night-shift work. These data suggest that further research is warranted and that high-risk occupations should be taken into consideration as public health policies are introduced and evolve.
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Project description:BackgroundChronic kidney disease patients show a high mortality in cases of a severe acute respiratory syndrome coronavirus-2 (SARS-CoV‑2) infection. Thus, information on the sero-status of nephrology personnel might be crucial for patient protection; however, limited information exists about the presence of SARS-CoV‑2 antibodies in asymptomatic individuals.MethodsWe examined the seroprevalence of SARS-CoV‑2 IgG and IgM antibodies among healthcare workers of a tertiary care kidney center during the the first peak phase of the corona virus disease 2019 (COVID-19) crisis in Austria using an orthogonal test strategy and a total of 12 commercial nucleocapsid protein or spike glycoprotein-based assays as well as Western blotting and a neutralization assay.ResultsAt baseline 60 of 235 study participants (25.5%, 95% confidence interval, CI 20.4-31.5%) were judged to be borderline positive or positive for IgM or IgG using a high sensitivity/low specificity threshold in one test system. Follow-up analysis after about 2 weeks revealed IgG positivity in 12 (5.1%, 95% CI: 2.9-8.8%) and IgM positivity in 6 (2.6%, 95% CI: 1.1-5.6) in at least one assay. Of the healthcare workers 2.1% (95% CI: 0.8-5.0%) showed IgG nucleocapsid antibodies in at least 2 assays. By contrast, positive controls with proven COVID-19 showed antibody positivity among almost all test systems. Moreover, serum samples obtained from healthcare workers did not show SARS-CoV‑2 neutralizing capacity, in contrast to positive controls.ConclusionUsing a broad spectrum of antibody tests the present study revealed inconsistent results for SARS-CoV‑2 seroprevalence among asymptomatic individuals, while this was not the case among COVID-19 patients.Trial registration numberCONEC, ClinicalTrials.gov number NCT04347694.
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Project description:ABO blood types could be a biological predisposition for depression. The present cross-sectional analysis was conducted amid the second wave of COVID-19 in Japan during July 2020. We wanted to investigate the association between ABO blood types and depressive symptoms among workers (352 men and 864 women, aged 21-73 years) of a medical institution in Tokyo, Japan, which took a leading role in the response to COVID-19 in the country. A Poisson regression model with a robust variance estimator was used to estimate the prevalence ratio (PR) and 95% confidence interval (CI) for depressive symptoms associated with ABO blood types. Overall, the prevalence of depressive symptoms (using two questions employed from a Two-question case-finding instrument) was 22.0%. The adjusted PRs (95% CI) for depressive symptoms, comparing the carriers of blood type O, A, and AB with those of type B, were 0.88 (0.66, 1.18), 0.81 (0.62, 1.07), and 1.07 (0.74, 1.53), respectively. There was no difference in the prevalence of depressive symptoms between non-B and B carriers. The present study did not support the association of ABO blood types with depressive symptoms.
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Project description:Individuals infected with the SARS-CoV-2 virus present with a wide variety of phenotypes ranging from asymptomatic to severe and even lethal outcomes. Past research has revealed a genetic haplotype on chromosome 3 that entered the human population via introgression from Neanderthals as the strongest genetic risk factor for the severe COVID-19 phenotype. However, the specific variants along this introgressed haplotype that contribute to this risk and the biological mechanisms that are involved remain unclear. Here, we assess the variants present on the risk haplotype for their likelihood of driving the severe COVID-19 phenotype. We do this by first exploring their impact on the regulation of genes involved in COVID-19 infection using a variety of population genetics and functional genomics tools. We then perform an locus-specific massively parallel reporter assay to individually assess the regulatory potential of each allele on the haplotype in a multipotent immune-related cell line. We ultimately reduce the set of over 600 linked genetic variants to identify 4 introgressed alleles that are strong functional candidates for driving the association between this locus and the severe COVID-19. These variants likely drive the locus’ impact on severity by putatively modulating the regulation of two critical chemokine receptor genes: CCR1 and CCR5. These alleles are ideal targets for future functional investigations into the interaction between host genomics and COVID-19 outcomes.
2023-02-09 | GSE176233 | GEO