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1.
Front Cell Infect Microbiol ; 11: 767771, 2021.
Article in English | MEDLINE | ID: covidwho-1526762

ABSTRACT

Background: ABO and Rh blood group systems are associated with many diseases including cancerous, infectious, non-infectious, bacterial and viral diseases. Studies have shown association of blood groups A and O with higher and lower odds for coronavirus disease 2019 positivity, respectively. Methods: This is a single-center, retrospective study conducted at Sir Ganga Ram Hospital, Delhi. We investigated the association of ABO and Rh blood groups with susceptibility to coronavirus disease 2019 infection, severity of disease, recovery period, and mortality of patients. Patients were enrolled from April 8, 2020 to October 4, 2020. A total of 2,586 real-time PCR (RT-PCR)-confirmed coronavirus disease 2019 (COVID-19) patients were recruited. Data was analyzed using chi-square test, odds ratio, and Mann-Whitney test to determine the association of blood groups. Results: In the 2,586 COVID-19-infected patients, the frequencies of A, B, O, and AB were 29.93%, 41.80%, 21.19%, and 7.98%, respectively. Of the patients, 98.07% were Rh positive. Blood group A (odds ratio, 1.53; CI, 1.40-1.66; p < 0.001) and B (odds ratio, 1.15; CI, 1.06-1.24; p < 0.001) is observed to be significantly associated with COVID-19 susceptibility, whereas blood group O (odds ratio, 0.65; CI, 0.59-0.71; p < 0.001) and AB (odds ratio, 0.66; CI, 0.59-0.71; p < 0.001) have low risk of COVID-19 infection. Conclusion: A, B, and Rh+ are found to be more susceptible to COVID-19 infection, whereas blood groups O, AB, and Rh- are at a lower risk of COVID-19 infection. No association was found between blood groups and susceptibility to severity of disease and mortality.


Subject(s)
COVID-19 , ABO Blood-Group System/genetics , Hospitals , Humans , India/epidemiology , Retrospective Studies , SARS-CoV-2
2.
Signal Transduct Target Ther ; 6(1): 344, 2021 09 20.
Article in English | MEDLINE | ID: covidwho-1428800

ABSTRACT

Coronavirus disease 2019 (COVID-19) caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in considerable morbidity and mortality worldwide. COVID-19 incidence, severity, and mortality rates differ greatly between populations, genders, ABO blood groups, human leukocyte antigen (HLA) genotypes, ethnic groups, and geographic backgrounds. This highly heterogeneous SARS-CoV-2 infection is multifactorial. Host genetic factors such as variants in the angiotensin-converting enzyme gene (ACE), the angiotensin-converting enzyme 2 gene (ACE2), the transmembrane protease serine 2 gene (TMPRSS2), along with HLA genotype, and ABO blood group help to explain individual susceptibility, severity, and outcomes of COVID-19. This review is focused on COVID-19 clinical and viral characteristics, pathogenesis, and genetic findings, with particular attention on genetic diversity and variants. The human genetic basis could provide scientific bases for disease prediction and targeted therapy to address the COVID-19 scourge.


Subject(s)
Angiotensin-Converting Enzyme 2/genetics , COVID-19/genetics , Peptidyl-Dipeptidase A/genetics , SARS-CoV-2/genetics , ABO Blood-Group System/genetics , COVID-19/epidemiology , COVID-19/virology , Female , Genotype , HLA Antigens/genetics , Humans , Male , Risk Factors , SARS-CoV-2/pathogenicity , Serine Endopeptidases/genetics
3.
Eur J Med Res ; 26(1): 107, 2021 Sep 16.
Article in English | MEDLINE | ID: covidwho-1412355

ABSTRACT

BACKGROUND: COVID-19, the pandemic disease caused by infection with SARS-CoV-2, may take highly variable clinical courses, ranging from symptom-free and pauci-symptomatic to fatal disease. The goal of the current study was to assess the association of COVID-19 clinical courses controlled by patients' adaptive immune responses without progression to severe disease with patients' Human Leukocyte Antigen (HLA) genetics, AB0 blood group antigens, and the presence or absence of near-loss-of-function delta 32 deletion mutant of the C-C chemokine receptor type 5 (CCR5). PATIENT AND METHODS: An exploratory observational study including 157 adult COVID-19 convalescent patients was performed with a median follow-up of 250 days. The impact of different HLA genotypes, AB0 blood group antigens, and the CCR5 mutant CD195 were investigated for their role in the clinical course of COVID-19. In addition, this study addressed levels of severity and morbidity of COVID-19. The association of the immunogenetic background parameters were further related to patients' humoral antiviral immune response patterns by longitudinal observation. RESULTS: Univariate HLA analyses identified putatively protective HLA alleles (HLA class II DRB1*01:01 and HLA class I B*35:01, with a trend for DRB1*03:01). They were associated with reduced durations of disease instead decreased (rather than increased) total anti-S IgG levels. They had a higher virus neutralizing capacity compared to non-carriers. Conversely, analyses also identified HLA alleles (HLA class II DQB1*03:02 und HLA class I B*15:01) not associated with such benefit in the patient cohort of this study. Hierarchical testing by Cox regression analyses confirmed the significance of the protective effect of the HLA alleles identified (when assessed in composite) in terms of disease duration, whereas AB0 blood group antigen heterozygosity was found to be significantly associated with disease severity (rather than duration) in our cohort. A suggestive association of a heterozygous CCR5 delta 32 mutation status with prolonged disease duration was implied by univariate analyses but could not be confirmed by hierarchical multivariate testing. CONCLUSION: The current study shows that the presence of HLA class II DRB1*01:01 and HLA class I B*35:01 is of even stronger association with reduced disease duration in mild and moderate COVID-19 than age or any other potential risk factor assessed. Prospective studies in larger patient populations also including novel SARS-CoV-2 variants will be required to assess the impact of HLA genetics on the capacity of mounting protective vaccination responses in the future.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/etiology , HLA Antigens/genetics , Receptors, CCR5/genetics , Adult , Aged , COVID-19/epidemiology , COVID-19/genetics , Female , Genetic Predisposition to Disease , Genotype , HLA-DRB1 Chains/genetics , Histocompatibility Antigens Class I/genetics , Humans , Immunoglobulin G/blood , Male , Middle Aged , Morbidity , Mutation , Severity of Illness Index
4.
Vox Sang ; 116(8): 849-861, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1402984

ABSTRACT

Growing evidence suggests that ABO blood group may play a role in the immunopathogenesis of SARS-CoV-2 infection, with group O individuals less likely to test positive and group A conferring a higher susceptibility to infection and propensity to severe disease. The level of evidence supporting an association between ABO type and SARS-CoV-2/COVID-19 ranges from small observational studies, to genome-wide-association-analyses and country-level meta-regression analyses. ABO blood group antigens are oligosaccharides expressed on red cells and other tissues (notably endothelium). There are several hypotheses to explain the differences in SARS-CoV-2 infection by ABO type. For example, anti-A and/or anti-B antibodies (e.g. present in group O individuals) could bind to corresponding antigens on the viral envelope and contribute to viral neutralization, thereby preventing target cell infection. The SARS-CoV-2 virus and SARS-CoV spike (S) proteins may be bound by anti-A isoagglutinins (e.g. present in group O and group B individuals), which may block interactions between virus and angiotensin-converting-enzyme-2-receptor, thereby preventing entry into lung epithelial cells. ABO type-associated variations in angiotensin-converting enzyme-1 activity and levels of von Willebrand factor (VWF) and factor VIII could also influence adverse outcomes, notably in group A individuals who express high VWF levels. In conclusion, group O may be associated with a lower risk of SARS-CoV-2 infection and group A may be associated with a higher risk of SARS-CoV-2 infection along with severe disease. However, prospective and mechanistic studies are needed to verify several of the proposed associations. Based on the strength of available studies, there are insufficient data for guiding policy in this regard.


Subject(s)
ABO Blood-Group System , COVID-19 , ABO Blood-Group System/genetics , Blood Grouping and Crossmatching , Humans , Prospective Studies , SARS-CoV-2
6.
PLoS One ; 16(8): e0256441, 2021.
Article in English | MEDLINE | ID: covidwho-1376626

ABSTRACT

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.


Subject(s)
ABO Blood-Group System , COVID-19/epidemiology , Depressive Disorder/diagnosis , Health Personnel/statistics & numerical data , ABO Blood-Group System/genetics , Adult , Aged , COVID-19/virology , Cross-Sectional Studies , Depressive Disorder/epidemiology , Disease Susceptibility/blood , Female , Genetic Predisposition to Disease , Humans , Japan , Male , Middle Aged , Pandemics , Prevalence , SARS-CoV-2/isolation & purification , Young Adult
7.
Genes (Basel) ; 12(7)2021 06 24.
Article in English | MEDLINE | ID: covidwho-1295801

ABSTRACT

ABO blood system is an inborn trait determined by the ABO gene. The genetic-phenotypic mechanism underneath the four mutually exclusive and collectively exhaustive types of O, A, B and AB could theoretically be elucidated. However, genetic polymorphisms in the human populations render the link elusive, and importantly, past studies using genetically determined rather than biochemically determined ABO types were not and could not be evaluated for the inference errors. Upon both blood-typing and genotyping a cohort of 1008 people of the Han Chinese population, we conducted a genome-wide association study in parallel with both binomial and multinomial log-linear models. Significant genetic variants are all mapped to the ABO gene, and are quantitatively evaluated for binary and multi-class classification performances. Three single nucleotide polymorphisms of rs8176719, rs635634 and rs7030248 would together be sufficient to establish a multinomial predictive model that achieves high accuracy (0.98) and F1 scores (micro 0.99 and macro 0.97). Using the set of identified ABO-associated genetic variants as instrumental variables, we demonstrate the application in causal analysis by Mendelian randomization (MR) studies on blood pressures (one-sample MR) and severe COVID-19 with respiratory failure (two-sample MR).


Subject(s)
ABO Blood-Group System/blood , ABO Blood-Group System/genetics , COVID-19/genetics , Polymorphism, Single Nucleotide , Adult , Blood Pressure/genetics , COVID-19/etiology , Cohort Studies , Female , Genetic Predisposition to Disease , Genome-Wide Association Study , Humans , Male , Mendelian Randomization Analysis , Middle Aged , Models, Statistical , Serologic Tests
8.
Transfus Apher Sci ; 60(4): 103169, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1240637

ABSTRACT

BACKGROUND: Numerous studies investigate the association between the ABO blood groups and the occurrence of COVID-19 infection; discordant findings were reported. Therefore, the purpose of this meta-analysis was to evaluate the existing evidence on the susceptibility of the ABO blood group to COVID-19 infection. METHODS: Systematically searched published articles in PubMed, Google Scholar, Scopus, and EMBASE between 1 st January 2020 and 21 st March 2021. After quality control and the exclusion of irrelevant studies, 16 studies were included in the final analysis. RESULTS: Although the random-effect meta-analysis revealed a large heterogeneity among studies, I 2 = 99.197 %. The pooled event rates and (95 % CIs) for A, O, B, and AB blood group were 0.459 (95 %CI: 0.358-0.441), 0.342 (95 %CI: 0.298-0.374), 0.180 (95 %CI: 0.150-0.214), and 0.076 (95 %CI: 0.055-0.127), respectively. These results indicated that the COVID-19 infection rate was higher in persons with blood group A > O > B > AB. Overall, the ABO blood group's vulnerability to COVID-19 infection was statistically significant (pooled p -value<0.001). CONCLUSION: This meta-analysis offers a further indication of blood group A individuals' vulnerability to COVID-19 infection, and blood type AB are linked to a lower risk of COVID-19 infection.


Subject(s)
ABO Blood-Group System/analysis , COVID-19/blood , Pandemics , SARS-CoV-2 , ABO Blood-Group System/genetics , COVID-19/genetics , Evidence-Based Medicine , Genetic Predisposition to Disease , Humans
9.
Arch Virol ; 166(8): 2089-2108, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1209235

ABSTRACT

The SARS-CoV-2 pandemic has become one of the most serious health concerns globally. Although multiple vaccines have recently been approved for the prevention of coronavirus disease 2019 (COVID-19), an effective treatment is still lacking. Our knowledge of the pathogenicity of this virus is still incomplete. Studies have revealed that viral factors such as the viral load, duration of exposure to the virus, and viral mutations are important variables in COVID-19 outcome. Furthermore, host factors, including age, health condition, co-morbidities, and genetic background, might also be involved in clinical manifestations and infection outcome. This review focuses on the importance of variations in the host genetic background and pathogenesis of SARS-CoV-2. We will discuss the significance of polymorphisms in the ACE-2, TMPRSS2, vitamin D receptor, vitamin D binding protein, CD147, glucose-regulated protein 78 kDa, dipeptidyl peptidase-4 (DPP4), neuropilin-1, heme oxygenase, apolipoprotein L1, vitamin K epoxide reductase complex 1 (VKORC1), and immune system genes for the clinical outcome of COVID-19.


Subject(s)
COVID-19/genetics , ABO Blood-Group System/genetics , Angiotensin-Converting Enzyme 2/genetics , Apolipoprotein L1/genetics , Basigin/genetics , COVID-19/epidemiology , COVID-19/therapy , Dipeptidyl Peptidase 4/genetics , Heat-Shock Proteins/genetics , Heme Oxygenase-1/genetics , Humans , Immunity/genetics , Neuropilin-1/genetics , Patient Outcome Assessment , Polymorphism, Genetic , Receptors, Calcitriol/genetics , SARS-CoV-2 , Serine Endopeptidases/genetics , Vitamin D-Binding Protein/genetics , Vitamin K Epoxide Reductases/genetics
10.
Nat Genet ; 53(6): 801-808, 2021 06.
Article in English | MEDLINE | ID: covidwho-1199301

ABSTRACT

COVID-19 presents with a wide range of severity, from asymptomatic in some individuals to fatal in others. Based on a study of 1,051,032 23andMe research participants, we report genetic and nongenetic associations with testing positive for SARS-CoV-2, respiratory symptoms and hospitalization. Using trans-ancestry genome-wide association studies, we identified a strong association between blood type and COVID-19 diagnosis, as well as a gene-rich locus on chromosome 3p21.31 that is more strongly associated with outcome severity. Hospitalization risk factors include advancing age, male sex, obesity, lower socioeconomic status, non-European ancestry and preexisting cardiometabolic conditions. While non-European ancestry was a significant risk factor for hospitalization after adjusting for sociodemographics and preexisting health conditions, we did not find evidence that these two primary genetic associations explain risk differences between populations for severe COVID-19 outcomes.


Subject(s)
COVID-19/genetics , Genetic Predisposition to Disease , ABO Blood-Group System/genetics , Blood Grouping and Crossmatching , Chromosomes, Human, Pair 3 , Databases, Genetic , Disease Susceptibility , Female , Galactosyltransferases/genetics , Genome-Wide Association Study , Hospitalization , Humans , Male , Middle Aged , Patient Acuity , Risk Factors
11.
Blood Cells Mol Dis ; 89: 102571, 2021 07.
Article in English | MEDLINE | ID: covidwho-1198629

ABSTRACT

BACKGROUND: A recent study showed that the ABO gene, chr 9q34.2, which determines blood type, may affect COVID-19 disease severity, although this result has not been reproducible. A UK study of 2200 COVID-19 patients found no relationship of ABO blood type to disease severity. A Danish study identified ABO blood group as a risk factor for SARS-CoV-2 infection but not for hospitalization or death from COVID-19. AIM: In the current study, we wished to analyze the relationship of ABO blood group and the ABO genetic locus to COVID-19 test positivity and mortality in subjects from the UK Biobank (UKB). METHODS: ABO blood type is from UKB data field 23165. Blood type was imputed for genotyped UK Biobank participants using three SNPs (rs505922, rs8176719, and rs8176746) in the ABO gene on chromosome 9q34.2. We analyzed the chromosome 9 snp rs657152 to assess the relationship of the ABO locus to COVID-19 test positivity and mortality. RESULTS: COVID-19 test results (negative or positive) were not related to blood group in males (p = 0.977, two tailed Fisher exact test) or females (p = 0.548). COVID-19 outcomes (alive or died) were not related to blood group in males (p = 0.102, two tailed Fisher exact test) or females (p = 0.226). We found no significant relationship of rs657152 to COVID-19 test positivity or mortality. CONCLUSION: We were not able to confirm that ABO blood group influences risk of COVID-19 infection or outcome.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/genetics , COVID-19/mortality , Polymorphism, Single Nucleotide , SARS-CoV-2 , Female , Humans , Male
12.
Ann Hematol ; 100(5): 1123-1132, 2021 May.
Article in English | MEDLINE | ID: covidwho-1122761

ABSTRACT

An association of various blood types and the 2019 novel coronavirus disease (COVID-19) has been found in a number of publications. The aim of this literature review is to summarize key findings related to ABO blood types and COVID-19 infection rate, symptom presentation, and outcome. Summarized findings include associations between ABO blood type and higher infection susceptibility, intubation duration, and severe outcomes, including death. The literature suggests that blood type O may serve as a protective factor, as individuals with blood type O are found COVID-19 positive at far lower rates. This could suggest that blood type O individuals are less susceptible to infection, or that they are asymptomatic at higher rates and therefore do not seek out testing. We also discuss genetic associations and potential molecular mechanisms that drive the relationship between blood type and COVID-19. Studies have found a strong association between a locus on a specific gene cluster on chromosome three (chr3p21.31) and outcome severity, such as respiratory failure. Cellular models have suggested an explanation for blood type modulation of infection, evidencing that spike protein/Angiotensin-converting enzyme 2 (ACE2)-dependent adhesion to ACE2-expressing cell lines was specifically inhibited by monoclonal or natural human anti-A antibodies, so individuals with non-A blood types, specifically O, or B blood types, which produce anti-A antibodies, may be less susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection due to the inhibitory effects of anti-A antibodies.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/genetics , ABO Blood-Group System/blood , Blood Grouping and Crossmatching , COVID-19/blood , COVID-19/diagnosis , COVID-19/etiology , Disease Susceptibility , Genetic Predisposition to Disease , Humans , Incidence , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index
13.
Eur J Hum Genet ; 29(6): 1019-1026, 2021 06.
Article in English | MEDLINE | ID: covidwho-1111983

ABSTRACT

Germline variants in genes involved in SARS-CoV-2 cell entry and in host innate immune responses to viruses may influence the susceptibility to infection. This study used whole-genome analyses of lung tissue to identify polymorphisms acting as expression quantitative trait loci (eQTLs) for 60 genes of relevance to SARS-CoV-2 infection susceptibility. The expression of genes with confirmed or possible roles in viral entry-replication and in host antiviral responses was studied in the non-diseased lung tissue of 408 lung adenocarcinoma patients. No gene was differently expressed by sex, but APOBEC3H levels were higher and PARP12 levels lower in older individuals. A total of 125 cis-eQTLs (false discovery rate < 0.05) was found to modulate mRNA expression of 15 genes (ABO, ANPEP, AP2A2, APOBEC3D, APOBEC3G, BSG, CLEC4G, DDX58, DPP4, FURIN, FYCO1, RAB14, SERINC3, TRIM5, ZCRB1). eQTLs regulating ABO and FYCO1 were found in COVID-19 susceptibility loci. No trans-eQTLs were identified. Genetic control of the expression of these 15 genes, which encode putative virus receptors, proteins required for vesicle trafficking, enzymes that interfere with viral replication, and other restriction factors, may underlie interindividual differences in risk or severity of infection with SARS-CoV-2 or other viruses.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/genetics , Galactosyltransferases/genetics , Genetic Predisposition to Disease , Microtubule-Associated Proteins/genetics , COVID-19/virology , Gene Expression Regulation/genetics , Humans , Immunity, Innate/genetics , Lung/metabolism , Lung/pathology , Polymorphism, Genetic , Quantitative Trait Loci/genetics , Receptors, Virus/genetics , SARS-CoV-2/genetics , SARS-CoV-2/pathogenicity
14.
Infect Genet Evol ; 90: 104751, 2021 06.
Article in English | MEDLINE | ID: covidwho-1062516

ABSTRACT

COVID-19 is the currently evolving viral disease worldwide. It mainly targets the respiratory organs, tissues and causes illness. A plethora of studies has been performing to bring proper treatment and prevent people from the infection. Likewise, susceptibility to some infectious diseases has been associated with blood group phenotypes. The co-relationship of blood group with the occurrence of SARS-CoV-2 infection and death has been examined in numerous studies. This review explained the described studies regarding the correlation of blood group and the other essential factors with COVID-19.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/epidemiology , COVID-19/etiology , Disease Susceptibility , Phenotype , SARS-CoV-2 , ABO Blood-Group System/chemistry , ABO Blood-Group System/immunology , ABO Blood-Group System/metabolism , Coronavirus/classification , Coronavirus/immunology , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , Humans , Protein Binding , Receptors, Virus/chemistry , Receptors, Virus/metabolism , SARS-CoV-2/immunology , SARS-CoV-2/physiology , Structure-Activity Relationship , Thromboplastin/metabolism , von Willebrand Factor/metabolism
15.
J Autoimmun ; 117: 102595, 2021 02.
Article in English | MEDLINE | ID: covidwho-1014585

ABSTRACT

BACKGROUND: Genetic variation at a multigene cluster at chromosome 3p21.31 and the ABO blood group have been associated with the risk of developing severe COVID-19, but the mechanism remains unclear. Complement activation has been associated with COVID-19 severity. OBJECTIVE: The aim of this study was to examine whether chromosome 3p21.31 and the ABO variants are linked to the activation of the complement cascade in COVID-19 patients. METHODS: We considered 72 unrelated European hospitalized patients with genetic data and evaluation of circulating C5a and soluble terminal complement complex C5b-9 (SC5b-9). Twenty-six (36.1%) patients carried the rs11385942 G>GA variant and 44 (66.1%) non-O blood group associated with increased risk of severe COVID-19. RESULTS: C5a and SC5-b9 plasma levels were higher in rs11385949 GA carriers than in non-carriers (P = 0.041 and P = 0.012, respectively), while C5a levels were higher in non-O group than in O group patients (P = 0.019). The association between rs11385949 and SC5b-9 remained significant after adjustment for ABO and disease severity (P = 0.004) and further correction for C5a (P = 0.018). There was a direct relationship between upper airways viral load and SC5b-9 in carriers of the rs11385949 risk allele (P = 0.032), which was not observed in non-carriers. CONCLUSIONS: The rs11385949 G>GA variant, tagging the chromosome 3 gene cluster variation and predisposing to severe COVID-19, is associated with enhanced complement activation, both with C5a and terminal complement complex, while non-O blood group with C5a levels. These findings provide a link between genetic susceptibility to more severe COVID-19 and complement activation.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/genetics , Chromosomes, Human, Pair 3/genetics , Complement Activation/genetics , Genotype , Multigene Family/genetics , Aged , Complement C5a/genetics , Disease Progression , Female , Gene Frequency , Genetic Association Studies , Genetic Predisposition to Disease , Hospitalization , Humans , Male , Middle Aged , Polymorphism, Single Nucleotide , Risk , SARS-CoV-2/physiology , Viral Load
16.
Genes (Basel) ; 12(1)2020 Dec 30.
Article in English | MEDLINE | ID: covidwho-1006317

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a fatal pandemic disease that is caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As of 13 December, 2020, over 70,000,000 cases and 1,500,000 deaths have been reported over a period of several months; however, the mechanism underlying the pathogenesis of COVID-19 has not been elucidated. To identify the novel risk genetic biomarker for COVID-19, we evaluated the correlation between the case fatality rate of COVID-19 and the genetic polymorphisms of several potential COVID-19-related genes, including interferon-induced transmembrane protein 3 (IFITM3), the angiotensin I converting enzyme 2 (ACE2) gene, transmembrane protease, serine 2 (TMPRSS2), interleukin 6 (IL6), leucine zipper transcription factor-like protein 1 (LZTFL1), and the ABO genes, in various ethnic groups. We obtained the number of COVID-19 cases and deaths from the World Health Organization (WHO) COVID-19 dashboard and calculated the case fatality rate of each ethnic group. In addition, we obtained the allele distribution of the polymorphisms of the IFITM3, ACE2, TMPRSS2, IL6, LZTFL1, and ABO genes from the 1000 Genomes Project and performed Log-linear regression analysis using SAS version 9.4. We found different COVID-19 case fatality rates in each ethnic group. Notably, we identified a strong correlation between the case fatality rate of COVID-19 and the allele frequency of the rs6598045 single nucleotide polymorphism (SNP) of the IFITM3 gene. To the best of our knowledge, this report is the first to describe a strong correlation between the COVID-19 case fatality rate and the rs6598045 SNP of the IFITM3 gene at the population-level.


Subject(s)
COVID-19/genetics , COVID-19/mortality , Membrane Proteins/genetics , RNA-Binding Proteins/genetics , SARS-CoV-2 , ABO Blood-Group System/genetics , Angiotensin-Converting Enzyme 2/genetics , Biomarkers , COVID-19/ethnology , Galactosyltransferases/genetics , Gene Frequency , Humans , Interleukin-6/genetics , Polymorphism, Single Nucleotide , Serine Endopeptidases/genetics , Severity of Illness Index , Transcription Factors/genetics
17.
Transplantation ; 105(1): 193-200, 2021 01 01.
Article in English | MEDLINE | ID: covidwho-990995

ABSTRACT

BACKGROUND: SARS-CoV-2 infection is heterogeneous in clinical presentation and disease evolution. To investigate whether immune response to the virus can be influenced by genetic factors, we compared HLA and AB0 frequencies in organ transplant recipients and waitlisted patients according to presence or absence of SARS-CoV-2 infection. METHODS: A retrospective analysis was performed on an Italian cohort composed by transplanted and waitlisted patients in a January 2002 to March 2020 time frame. Data from this cohort were merged with the Italian registry of COVID+ subjects, evaluating infection status of transplanted and waitlisted patients. A total of 56 304 cases were studied with the aim of comparing HLA and AB0 frequencies according to the presence (n = 265, COVID+) or absence (n = 56 039, COVID-) of SARS-CoV-2 infection. RESULTS: The cumulative incidence rate of COVID-19 was 0.112% in the Italian population and 0.462% in waitlisted/transplanted patients (OR = 4.2; 95% CI, 3.7-4.7; P < 0.0001). HLA-DRB1*08 was more frequent in COVID+ (9.7% and 5.2%: OR = 1.9, 95% CI, 1.2-3.1; P = 0.003; Pc = 0.036). In COVID+ patients, HLA-DRB1*08 was correlated to mortality (6.9% in living versus 17.5% in deceased: OR = 2.9, 95% CI, 1.15-7.21; P = 0.023). Peptide binding prediction analyses showed that these DRB1*08 alleles were unable to bind any of the viral peptides with high affinity. Finally, blood group A was more frequent in COVID+ (45.5%) than COVID- patients (39.0%; OR = 1.3; 95% CI, 1.02-1.66; P = 0.03). CONCLUSIONS: Although preliminary, these results suggest that HLA antigens may influence SARS-CoV-2 infection and clinical evolution of COVID-19 and confirm that blood group A individuals are at greater risk of infection, providing clues on the spread of the disease and indications about infection prognosis and vaccination strategies.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/etiology , HLA Antigens/genetics , Polymorphism, Genetic , SARS-CoV-2 , Adult , Aged , COVID-19/genetics , Female , Gene Frequency , Genetic Predisposition to Disease , Humans , Logistic Models , Male , Middle Aged , Retrospective Studies , Severity of Illness Index
18.
Blood Rev ; 48: 100785, 2021 07.
Article in English | MEDLINE | ID: covidwho-973900

ABSTRACT

The 2019 coronavirus disease (COVID-19) has become a global pandemic. Several studies report that ABO blood group polymorphism may be related to COVID-19 susceptibility and clinical outcomes; however, the results are controversial. We conducted a systematic review and meta-analysis to investigate whether ABO blood groups are associated with increased COVID-19 morbidity and mortality. A total of 715 articles were retrieved from seven databases. Ten articles were selected for meta-analysis after removal of duplicates and two levels of screenings. Overall, individuals with blood group A [odds ratio (OR) = 1.33, 95% confidence interval (CI) 1.14 to 1.56] and B (OR = 1.06, 95% CI 1.00 to 1.13) had a substantially higher risk of COVID-19, whereas this was not the case for blood group AB (OR = 1.07, 95% CI 0.88 to 1.30). Individuals with blood group O was not prone to develop the disease (OR = 0.71, 95% CI 0.60 to 0.84). Moreover, the risk of COVID-19 was significantly associated with the Rh-positive blood group (OR = 1.22, 95% CI 0.99 to 1.50). A meta-analysis of 5 studies suggested that blood group A was associated with a significantly increased risk of COVID-19 mortality (OR = 1.25, 95% CI 1.02 to 1.52). Mild publication bias was found in the included studies. This systematic review and meta-analysis indicated that blood groups A and B may be risk factors for COVID-19, whereas the blood group O appears to be protective. Blood group A may be related to unfavourable outcomes. Further rigorous and high-quality research evidence is needed to confirm this association.


Subject(s)
ABO Blood-Group System/genetics , COVID-19/blood , Pandemics , SARS-CoV-2 , COVID-19/epidemiology , COVID-19/genetics , Case-Control Studies , Genetic Predisposition to Disease , Humans , Odds Ratio , Retrospective Studies , Rh-Hr Blood-Group System/genetics , Risk , Survival Analysis
19.
Haematologica ; 105(12): 2706-2708, 2020 12 01.
Article in English | MEDLINE | ID: covidwho-951560
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