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      ABO blood group is associated with COVID-19 susceptibility: a systematic review and meta-analysis

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          Abstract

          Abstract Introduction: Conflicting evidences exist that ABO blood groups correlate with the susceptibility to COVID-19 and its clinical outcomes. This study aimed to pool available articles that assessed a possible relationship between COVID-19 and ABO blood groups. Materials and methods: A search was conducted in four databases comprising Pubmed/Medline, Google scholar, Journal storage (JSTOR) and African Journals Online (AJOL) for relevant studies available before 25th August 2020 and contained extractable data on ABO blood type distribution and COVID-19 disease. Search terms included a combination of “ABO blood group, and COVID-19, coronavirus, and SARS-COV-2”. Results: Fourteen articles that met study inclusion criteria were selected from a total of five hundred and eighty-five articles identified through database search. The fourteen articles reviewed comprised of a total of 73934 subjects (13189 SARS-COV-2 positive cases and 60745 controls). Overall, the risk of SARS-COV-2 infection was found to be significantly increased in patients with blood group A with ORs: 1.24 (95%Cl: 1.09-1.41, P = 0.001). Additionally, blood group O subjects were seen to have decreased odds of contracting COVID-19 infection (OR: 0.78, 95%Cl: 0.68 – 0.89, P=0.0003). No significant association was found between ABO blood groups and COVID -19 severity and mortality. Conclusions: Blood group A was associated with a higher risk of SARS-COV-2 infection whereas risk of infection was lower in blood group O subjects. No statistical significant association was found between ABO blood groups and COVID-19 severity and mortality. The precise role of ABO blood group in COVID-19 susceptibility, severity and mortality requires further research for clarification.

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          Most cited references49

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          Risk factors of critical & mortal COVID-19 cases: A systematic literature review and meta-analysis

          Background An epidemic of Coronavirus Disease 2019 (COVID-19) began in December 2019 and triggered a Public Health Emergency of International Concern (PHEIC). We aimed to find risk factors for the progression of COVID-19 to help reducing the risk of critical illness and death for clinical help. Methods The data of COVID-19 patients until March 20, 2020 were retrieved from four databases. We statistically analyzed the risk factors of critical/mortal and non-critical COVID-19 patients with meta-analysis. Results Thirteen studies were included in Meta-analysis, including a total number of 3027 patients with SARS-CoV-2 infection. Male, older than 65, and smoking were risk factors for disease progression in patients with COVID-19 (male: OR = 1.76, 95% CI (1.41, 2.18), P 40U/L, creatinine(Cr) ≥ 133mol/L, hypersensitive cardiac troponin I(hs-cTnI) > 28pg/mL, procalcitonin(PCT) > 0.5ng/mL, lactatede hydrogenase(LDH) > 245U/L, and D-dimer > 0.5mg/L predicted the deterioration of disease while white blood cells(WBC) 40U/L:OR=4.00, 95% CI (2.46, 6.52), P 28 pg/mL: OR = 43.24, 95% CI (9.92, 188.49), P 0.5 ng/mL: OR = 43.24, 95% CI (9.92, 188.49), P 245U/L: OR = 43.24, 95% CI (9.92, 188.49), P 0.5mg/L: OR = 43.24, 95% CI (9.92, 188.49), P < 0.00001; WBC < 4 × 109/L: OR = 0.30, 95% CI (0.17, 0.51), P < 0.00001]. Conclusion Male, aged over 65, smoking patients might face a greater risk of developing into the critical or mortal condition and the comorbidities such as hypertension, diabetes, cardiovascular disease, and respiratory diseases could also greatly affect the prognosis of the COVID-19. Clinical manifestation such as fever, shortness of breath or dyspnea and laboratory examination such as WBC, AST, Cr, PCT, LDH, hs-cTnI and D-dimer could imply the progression of COVID-19.
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            Genomewide Association Study of Severe Covid-19 with Respiratory Failure

            Abstract Background There is considerable variation in disease behavior among patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (Covid-19). Genomewide association analysis may allow for the identification of potential genetic factors involved in the development of Covid-19. Methods We conducted a genomewide association study involving 1980 patients with Covid-19 and severe disease (defined as respiratory failure) at seven hospitals in the Italian and Spanish epicenters of the SARS-CoV-2 pandemic in Europe. After quality control and the exclusion of population outliers, 835 patients and 1255 control participants from Italy and 775 patients and 950 control participants from Spain were included in the final analysis. In total, we analyzed 8,582,968 single-nucleotide polymorphisms and conducted a meta-analysis of the two case–control panels. Results We detected cross-replicating associations with rs11385942 at locus 3p21.31 and with rs657152 at locus 9q34.2, which were significant at the genomewide level (P<5×10−8) in the meta-analysis of the two case–control panels (odds ratio, 1.77; 95% confidence interval [CI], 1.48 to 2.11; P=1.15×10−10; and odds ratio, 1.32; 95% CI, 1.20 to 1.47; P=4.95×10−8, respectively). At locus 3p21.31, the association signal spanned the genes SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6 and XCR1. The association signal at locus 9q34.2 coincided with the ABO blood group locus; in this cohort, a blood-group–specific analysis showed a higher risk in blood group A than in other blood groups (odds ratio, 1.45; 95% CI, 1.20 to 1.75; P=1.48×10−4) and a protective effect in blood group O as compared with other blood groups (odds ratio, 0.65; 95% CI, 0.53 to 0.79; P=1.06×10−5). Conclusions We identified a 3p21.31 gene cluster as a genetic susceptibility locus in patients with Covid-19 with respiratory failure and confirmed a potential involvement of the ABO blood-group system. (Funded by Stein Erik Hagen and others.)
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              Linkage disequilibrium in the human genome.

              With the availability of a dense genome-wide map of single nucleotide polymorphisms (SNPs), a central issue in human genetics is whether it is now possible to use linkage disequilibrium (LD) to map genes that cause disease. LD refers to correlations among neighbouring alleles, reflecting 'haplotypes' descended from single, ancestral chromosomes. The size of LD blocks has been the subject of considerable debate. Computer simulations and empirical data have suggested that LD extends only a few kilobases (kb) around common SNPs, whereas other data have suggested that it can extend much further, in some cases greater than 100 kb. It has been difficult to obtain a systematic picture of LD because past studies have been based on only a few (1-3) loci and different populations. Here, we report a large-scale experiment using a uniform protocol to examine 19 randomly selected genomic regions. LD in a United States population of north-European descent typically extends 60 kb from common alleles, implying that LD mapping is likely to be practical in this population. By contrast, LD in a Nigerian population extends markedly less far. The results illuminate human history, suggesting that LD in northern Europeans is shaped by a marked demographic event about 27,000-53,000 years ago.
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                Author and article information

                Journal
                ijm
                Iberoamerican Journal of Medicine
                Iberoam J Med
                Hospital San Pedro (Logroño, La Rioja, Spain )
                2695-5075
                2695-5075
                2021
                : 3
                : 1
                : 71-84
                Affiliations
                [8] Abakaliki orgnameAlex Ekwueme Federal University Teaching Hospital orgdiv1Department of Engineering and Maintenance Nigeria
                [4] Abakaliki Ebonyi orgnameEbonyi State University orgdiv1College of Health Sciences orgdiv2Faculty of Clinical Medicine. Department of Haematology and Immunology Nigeria
                [7] Abakaliki orgnameAlex Ekwueme Federal University Teaching Hospital orgdiv1Department of Community Medicine Nigeria
                [6] Abakaliki Ebonyi orgnameEbonyi State University orgdiv1College of Health Science orgdiv2Department of Community Medicine Nigeria
                [3] Jos orgnameFederal School of Medical Laboratory Science orgdiv1Department of Medical Laboratory Management Nigeria
                [1] Abakaliki orgnameAlex Ekwueme Federal University Teaching Hospital orgdiv1Department of Medical Laboratory Services Nigeria
                [2] Abakaliki Ebonyi orgnameEbonyi State University orgdiv1Faculty of Medicine orgdiv2Department of Pediatrics Nigeria
                [5] Jos orgnameFederal School of Medical Laboratory Science orgdiv1Department of Haematology & Blood Transfusion Science Nigeria
                Article
                S2695-50752021000100012 S2695-5075(21)00300100012
                10.5281/zenodo.4344131
                db71b338-c4ae-48d8-b920-a9278795ca26

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 17 December 2020
                : 24 September 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 49, Pages: 14
                Product

                SciELO Spain

                Categories
                Review

                COVID-19,SARS-COV-2,Mortality,Severity,Susceptibility,ABO blood group

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