ABO blood group association and COVID-19. COVID-19 susceptibility and severity: a review

Shibeeb, Sapha; Khan, Aisha Saleem

doi:10.1016/j.htct.2021.07.006

Cited by 31 publications

(28 citation statements)

References 47 publications

(57 reference statements)

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“…Secondly, it is a single-center study, on a Caucasian population, and the results may not be extrapolated to other populations. The frequencies of the ABO groups in the studied population are a confounding factor since geographical variations constitute potential bias [6]. In our case, the blood group proportions have been very similar to those in Spain (43.3% group A, 43.3% group O, and 13.4% groups B+AB).…”

Section: Potential Implications Of the Resultssupporting

confidence: 72%

“…This finding has been related to the anti-A antibodies presented in blood group O individuals. These antibodies bind themselves to the A-like antigens or to the spike protein expressed on the virus envelope, blocking its interaction with the ACE-2 receptor, which is an identified gateway for different coronaviruses to infect host cells [6].…”

Section: Introductionmentioning

confidence: 99%

“…Regarding clinical outcomes, blood group A has been associated with a higher risk of hospitalization, mechanical ventilation, and death [6,7]. These adverse outcomes have been related to higher levels of soluble circulating proteins linked to vascular adhesion in people with this group [8].…”

Section: Introductionmentioning

confidence: 99%

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Blood group O and post-COVID-19 syndrome

Díaz-Salazar

Navas

Sainz-Maza

et al. 2022

Preprint

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Objective The ABO system modulates the inflammatory response, and it has been involved in SARS-CoV-2 infection. There is increasing evidence of underlying immune-inflammatory mechanisms in post-COVID-19 syndrome (PCS). Blood group O seems to protect against COVID-19 infection, but there is no data on the relationship between blood group O and PCS. This study aimed to assess this potential association. Subjects and methods A case-control study including subjects who had suffered from mild COVID-19 in a community setting was designed. Cases were PCS+ patients, controls were PCS- subjects and the exposure variable was blood group O. Baseline epidemiological data (age, sex, BMI, smoking, comorbidities), and clinical and laboratory parameters (inflammatory markers and IgG anti-N antibodies) 3 months after the acute episode, were obtained. Five composite indices of inflammation were built, combining the upper ranges of the distributions of inflammatory markers. Blood group and Rh factor were obtained from the patient's medical history or capillary blood samples. Bivariate and multivariate analyses were performed. Results One-hundred and twenty-one subjects were analyzed (56.2% women). The mean age was 45.7 (16) years (range, 18-88 years). Blood group frequencies were 43.3% (group A), 7.7% (group B), 5.7% (group AB), and 43.3% (group O). Thirty-six patients were classified as PCS+ (25 women, 11 men; p=0.07). The most frequent symptom was fatigue (42.8%). There were no significant differences between PCS+ and PCS- subjects regarding age, BMI, smoking, or previous comorbidity. The prevalence of PCS was 43.2% (19/44) in the blood group O and 23.7% in non-O subjects (14/60) (p=0.036). The mean number of PCS symptoms was 0.82 (1) in the blood group O and 0.43 (0.9) in the non-O group (p=0.017). There were no significant differences between A, B, and AB groups (PCS+ and PCS-) regarding inflammatory markers. In contrast, blood group O PCS+ patients had significantly higher lymphocyte count, plasma CRP, fibrinogen levels, and higher percentages of C2, C3, and C4 composite indices than PCS- subjects. The blood group O had an increased risk of developing PCS compared to non-O subjects (adjusted OR=4.20 [95%CI, 1.2-14]; p=0.023). The variables that contributed the most to the predictive model were blood group O, lymphocyte count, neutrophil count, and female sex. R-squared was 0.46, and the area under the ROC curve was 0.807 [95% CI, 0.70-0.90] (p=0.0001). Conclusion An increased risk of PCS associated with blood group O has been observed. Slightly, albeit significant, raised levels of fibrinogen, CRP, and neutrophil and lymphocyte counts, not observed in the other ABO blood groups, have been demonstrated in blood group O. Further investigations are needed to confirm these results.

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Section: Potential Implications Of the Resultssupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

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Blood group O and post-COVID-19 syndrome

Díaz-Salazar

Navas

Sainz-Maza

et al. 2022

Preprint

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“…Some contrasting literature data were reported on the specific subjects' different susceptibility to the viral attack, based on determined genetic mutations, blood groups/diseases, specific receptors expression. 71,191,309,[348][349][350][351][352][353][354][355] Beyond a specific possible TMPRSS2-related predisposition on a genetic or epigenetic (e.g. diabetic and obese patients) basis, 356 the majority of these speculations refer both to the variability of the membrane expression of certain receptors (namely SA and CD147), and to the consequent cation dysmetabolism.…”

Section: Discussionmentioning

confidence: 99%

COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

et al. 2022

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Background: iron and calcium dysmetabolism, with hyperferritinemia, hypoferremia, hypocalcemia and anemia have been documented in the majority of COVID-19 patients at later/worse stages. Furthermore, complementary to ACE2, both sialic acid (SA) molecules and CD147 proved relevant host receptors for SARS-CoV-2 entry, which explains the viral attack to multiple types of cells, including erythrocytes, endothelium and neural tissue. Several authors advocated that cell ferroptosis may be the core and final cell degenerative mechanism. Methods: a literature research was performed in several scientific search engines, such as PubMed Central, Cochrane Library, Chemical Abstract Service. More than 500 articles were retrieved until mid-December 2021, to highlight the available evidence about the investigated issues. Results: based on COVID-19 literature data, we have highlighted a few pathophysiological mechanisms, associated with virus-based cation dysmetabolism, multi-organ attack, mitochondria degeneration and ferroptosis. Our suggested elucidated pathological sequence is: a) spike protein subunit S1 docking with sialylated membrane glycoproteins/receptors (ACE2, CD147), and S2 subunit fusion with the lipid layer; b) cell membrane morpho-functional changes due to the consequent electro-chemical variations and viroporin action, which induce an altered ion channel function and intracellular cation accumulation; c) additional intracellular iron concentration due to a deregulated hepcidin-ferroportin axis, with higher hepcidin levels. Viral invasion may also affect erythrocytes/erythroid precursors, endothelial cells and macrophages, through SA and CD147 receptors, with relative hemoglobin and iron/calcium dysmetabolism. AB0 blood group, hemochromatosis, or environmental elements may represent possible factors which affect individual susceptibility to COVID-19. Conclusions: our literature analysis confirms the combined role of SA molecules, ACE2, CD147, viroporins and hepcidin in determining the cation dysmetabolism and final ferroptosis in the cells infected by SARS-CoV-2. The altered ion channels and electrochemical gradients of the cell membrane have a pivotal role in the virus entry and cell dysmetabolism, with subsequent multi-organ immune-inflammatory degeneration and erythrocyte/hemoglobin alterations.

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“…On the one hand, the S protein could be decorated with A or B carbohydrate epitopes able to be recognized by the natural anti-A or -B antibodies from blood group O, B, and A individuals ( 24 ). On the other hand, natural anti-A or -B antibodies can directly bind to the ACE2 glycosylated region ( 43 ). In this case, possible competitive inhibition of ACE2 by both natural (anti-A/anti-B) antibodies and SARS-CoV-2 may induce early ACE2 downregulation in blood group O, increasing the production of multiple inflammatory cytokines ( 44 ) in the first step of the infection.…”

Section: Relationship Between Abo Blood Group and Covid-19 Severity A...mentioning

confidence: 99%

ABO Blood System and COVID-19 Susceptibility: Anti-A and Anti-B Antibodies Are the Key Points

et al. 2022

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The implication of the ABO blood group in COVID-19 disease was formulated early, at the beginning of the COVID-19 pandemic more than 2 years ago. It has now been established that the A blood group is associated with more susceptibility and severe symptoms of COVID-19, while the O blood group shows protection against viral infection. In this review, we summarize the underlying pathophysiology of ABO blood groups and COVID-19 to explain the molecular aspects behind the protective mechanism in the O blood group. A or B antigens are not associated with a different risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection than that of other antigens. In this case, the cornerstone is natural anti-A and anti-B antibodies from the ABO system. They are capable of interfering with the S protein (SARS-CoV-2) and angiotensin-converting enzyme 2 (ACE2; host cell receptor), thereby conferring protection to patients with sufficient antibodies (O blood group). Indeed, the titers of natural antibodies and the IgG isotype (specific to the O blood group) may be determinants of susceptibility and severity. Moreover, older adults are associated with a higher risk of bad outcomes due to the lack of antibodies and the upregulation of ACE2 expression during senescence. A better understanding of the role of the molecular mechanism of ABO blood groups in COVID-19 facilitates better prognostic stratification of the disease. Furthermore, it could represent an opportunity for new therapeutic strategies.

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ABO blood group association and COVID-19. COVID-19 susceptibility and severity: a review

Cited by 31 publications

References 47 publications

Blood group O and post-COVID-19 syndrome

Blood group O and post-COVID-19 syndrome

COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

ABO Blood System and COVID-19 Susceptibility: Anti-A and Anti-B Antibodies Are the Key Points

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