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Article

Association of ABO Blood Type with Infection and Severity of COVID-19 in Inpatient and Longitudinal Cohorts

by
Tiffany Eatz
1,*,
Alejandro Max Antonio Mantero
1,
Erin Williams
2,3,
Charles J. Cash
1,
Nathalie Perez
1,
Zachary J. Cromar
1,
Adiel Hernandez
1,
Matthew Cordova
1,
Neha Godbole
1,
Anh Le
1,
Rachel Lin
1,
Sherry Luo
1,
Anmol Patel
1,
Yaa Abu
1,
Suresh Pallikkuth
1 and
Savita Pahwa
1
1
Department of Microbiology & Immunology, University of Miami Miller School of Medicine, Miami, FL 33136, USA
2
Department of Otolaryngology, University of Miami Miller School of Medicine, Miami, FL 33136, USA
3
Department of Biomedical Engineering, University of Miami, Miami, FL 33136, USA
*
Author to whom correspondence should be addressed.
COVID 2023, 3(9), 1429-1439; https://doi.org/10.3390/covid3090098
Submission received: 7 August 2023 / Revised: 5 September 2023 / Accepted: 12 September 2023 / Published: 14 September 2023
Browse Figures
Versions Notes

Abstract

:
The objectives of this study were to (1) investigate the association between human blood type and COVID-19 in both inpatient and longitudinal populations and (2) identify the association between blood type and severity of COVID-19 via presence of cellular biomarkers of severe infection in hospitalized individuals at our institution in South Florida. This study consisted of (1) a single-center retrospective analysis of 669 out of 2741 COVID-19-positive, screened patients seen from 1 January 2020 until 31 March 2021 at the University of Miami Emergency Department (ED) who tested positive for COVID-19 and had a documented ABO blood type and (2) a longitudinal SARS-CoV-2 immunity study (“CITY”) at the University of Miami Miller School of Medicine, consisting of 185 survey participants. In an inpatient setting, blood type appeared to be associated with COVID-19 severity and mortality. Blood type O sustained less risk of COVID-19 mortality, and blood type O- demonstrated less risk of developing COVID-19 pneumonia. Inpatients with O- blood type exhibited less biomarkers of severe infection than did other blood types. In a longitudinal setting, there was no association found between blood type and SARS-CoV-2 infection.

1. Introduction

Blood type is a well-studied and well-established risk factor of a wide variety of conditions and may be considered when conducting research on different disease processes. The known effects of blood type in a disease’s process include thromboembolism, gastric ulcers, and malignancy, among others [1,2,3]. In the domain of infectious disease, blood type is a well-known risk factor [4] that correlates with clinical outcomes in parasitic, bacterial, and viral infections [5,6,7,8]. It has been postulated that human blood type may play a role in altering a patient’s susceptibility to SARS-CoV-2 infection.
The role of blood type is multifaceted in the overall process of infection [4]. For viral infections in particular, glycoproteins found on the surfaces of red blood cells serve as receptors for exogenous ligands that allow viral entry into the host cell [9]. With respect to SARS-CoV-2, the biochemical mechanism of entry is facilitated by viral S-protein binding to the metallocarboxyl peptidase angiotensin receptor (ACE-2) [10]. It is theorized that this viral entry is influenced by monoclonal or natural human anti-A antibodies specifically inhibiting the ACE-2-dependent binding of the viral S protein. This process is believed to lead individuals with non-A blood types (type O and B), which produce anti-A antibodies, to exhibit less susceptibility to SARS-CoV-2 infection due to the inhibitory effects of anti-A antibodies [11].
Furthermore, a meta-analysis performed by Wang et al., [12] which described the clinical correlation between blood type and COVID-19, found that type A and AB were more susceptible to infection, whereas type O was less susceptible. However, the lower risk of COVID-19 in patients with blood type O, but not type B, would contradict the aforementioned anti-A antibody protective mechanism, as both type O and B have anti-A antibodies. This contradiction paves the way for the generation of new hypotheses specific to the protective mechanism of solely blood type O.
It has also been demonstrated that rhesus (Rh) blood group status might play a protective role in COVID-19, specifically in that Rh negative blood groups may be associated with a lower risk of SARS-CoV-2 infection and severity [13]. Additional studies have found that Rh positivity may predispose an individual to a heightened risk [14].
As the pattern of blood type is geographically heterogenic, blood type is believed to play a role in epidemiological distribution of the pandemic [15]. These observed geographical trends in COVID-19 in association with blood type have been well documented [16]. Contrarily, other studies have found no significant association between blood group and SARS-CoV-2-associated infection, severity, mortality, nor hematological or radiological abnormalities [17,18]. To our knowledge, there has not yet been an analysis of the association between blood type and COVID-19 in a South Florida population.
ABO blood type may have an effect on the expression of biomarkers that indicate COVID-19 severity. Studies have highlighted the role of inflammatory response to infection with SARS-CoV-2 as a driving factor in disease outcome [19]. Three described pathological inflammatory processes induced by the SARS-CoV-2 virus include host (1) local manifestations of classical general (canonical) inflammation, (2) acute systemic inflammation, and (3) chronic systemic inflammation of low intensity [20,21]. Increases in these processes, respectively, coincide with exacerbated acute infection and negative long-term outcomes [20,21]. Rapid viral replication of SARS-CoV-2 results in cellular destruction, causing subsequent recruitment of macrophages and monocytes, and inducing the release of both cytokines and chemokines [22]. This release of cytokines and chemokines activating immune responses by signaling various immune cells could potentially lead to cytokine storms [23]. The levels of inflammatory acute phase proteins, S100A8, S100A9, SAA1, and SAA2, in COVID-positive individuals have been found to correlate with COVID-19 severity [24]. Evidence suggests that elevations in inflammatory markers, such as interleukin-6 (IL-6), serum ferritin, procalcitonin (PCT), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), are significantly associated with heightened severity of COVID-19 [25,26,27].
The objectives of this study were to (1) investigate the association between human blood type and COVID-19 in both inpatient and longitudinal populations and (2) identify the association between blood type and severity of COVID-19 via levels of cellular biomarkers of severe infection in hospitalized individuals at the University of Miami Health System: our institution in South Florida.

2. Methods

2.1. Retrospective Study Design and Participants

We conducted an IRB-approved (ID# 20210025) single-center retrospective analysis of admitted patients seen from 1 January 2020 to 31 March 2021 at the University of Miami Hospital Emergency Department (ED), who tested positive for COVID-19, regardless of reason for admission, and had a documented ABO blood type. Overall, 2741 COVID-19-positive patient charts were screened; 2072 individuals were excluded due to a lack of blood type data on file, yielding a total of 669 patients included in our statistical analyses. The following were also acquired from electronic medical records when available: demographics (sex and age), respiratory status (baseline, minimum, and maximum SpO2, ventilator use and diagnosis of pneumonia), and clinical biomarker test results (presence of abnormal monocytes, lymphocytes, megakaryocytes, and neutrophils on blood smear, percent and absolute neutrophils, monocytes, lymphocytes, eosinophils, and basophils, D-dimer, troponin, CRP, ferritin, lactate dehydrogenase (LDH), hemoglobin, hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW), platelets, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), creatinine, IL-6, IL-6 > 35 pg/mL, creatinine kinase, PCT, PCT of 0.5–2.0 ng/mL, PCT > 2.0 ng/mL, hemoglobinuria, hematuria, and age at time of death, as appropriate). If multiple values (i.e., from complete blood count) were input in a patient’s chart during their hospital visit, the most abnormal (most maximal or minimal) value was recorded for our study. Outcomes were measured as follows: development of COVID-19 pneumonia, ventilator use, diagnosis of acute respiratory distress syndrome (ARDS), and associated mortality.

2.2. Inpatient Cohort Statistical Analysis

For each blood type, the COVID-19 outcome rates and 95% confidence intervals were calculated to make comparisons between blood types with each of the clinical outcomes of interest. Comparisons were made using Chi-squared tests for categorical variables and ANOVA for continuous values (a = 0.05 significance level). All analyses were performed in R version 4.1.1. [28].

2.3. Longitudinal Cohort Study Design and Participants

We included 185 participants enrolled in our IRB-approved (#20201026), longitudinal SARS-CoV-2 immunity study (“CITY”) at the University of Miami Miller School of Medicine. This longitudinal cohort consisted of unique COVID positive and negative individuals that were not part of the 2741 originally screened patients. Following written informed consent, participants answered a demographic and health history questionnaire, which included disclosure of previous SARS-CoV-2 infection and blood type. All participants agreed to sample banking and consented to use in future research. For those with an unknown blood type at entry, typing was performed according to manufacturer instructions (Eldon Biologicals A/S) upon sample availability.

2.4. Longitudinal Cohort Statistical Analysis

Chi-squared tests were used to examine associations between COVID status and ABO or Rh blood grouping. All prospective analyses and figures were generated in R Studio [28].

3. Results

3.1. Inpatient Cohort Results

Our inpatient cohort had a mean age of 53.6 (±17.9) years with 48% males (n = 321) and 52% females (n = 348). The most common blood type was O (52.6%, n = 352), followed by A (35.3%, n = 236), B (10.8%, n = 72), and AB (1.3%, n = 9) (Table 1). Of patients with blood type O, 52.6% (confidence interval (CI): 47.2–57.9%) were female, and 47.4% (CI: 42.1–52.8%) were male. Of patients with blood type A, 50.8% (CI: 44.3–57.4%) were female, and 49.2% (CI: 42.6–55.7%) were male (Table 1). Of individuals with blood type B, 51.4% (CI: 39.3–63.3%) were female, and 48.6% (CI: 36.7–60.7%) were male; 66.7% (CI: 29.9–92.5%) of blood type AB patients were female, and 33.3% (CI: 7.49–70.1%) were male (Table 1). Of patients with blood type O, 86.6% were Rh positive (n = 305), and 13.4% (n = 47) were Rh negative. Of patients with blood type A, 88.6% (n = 209) were Rh positive, and 11.4% were Rh negative (n = 27). All (100%) of the patients with blood type AB (n = 9) as well as blood type B (n = 72) were Rh positive. All patients in this study presented to the ED with similar SpO2 values, with a mean SpO2 of 95.79% (SD, 0.47). Of the investigated outcomes, blood type O—patients demonstrated less risk of developing COVID-19 pneumonia (26.7% for O— vs. 69.2% for type A—, 56.5% for A+, 71.4% for AB+, 53.7% for B+, 51.5% for O+, and p-value = 0.003 via Chi-squared test) (Table 2). Blood type O, Rh negative or positive, exhibited decreased mortality due to COVID-19 when compared to other types (17.0% mortality for O vs. 26.3% for A, 29.2% for B, p-value = 0.012 via Chi-squared test) (Figure 1). We also assessed the association of blood type with biomarkers of severe COVID-19 for significant difference among blood groups, including Rh factor. O— demonstrated less elevated levels of LDH than did other blood types (p-value = 0.001, ANOVA) (Figure 1). O— demonstrated a higher frequency of clinically accepted baseline levels of troponin (<0.04 ng/mL) (p-value = 0.026, ANOVA) (Figure 1). Therefore, O— had less biomarkers indicative of a severe SARS-CoV-2 infection, which may coincide with the lower mortality rate of blood type O—.
Additional findings regarding general non-Rh-factor blood type were as follows: blood type O (Rh negative or positive) exhibited decreased levels of MCH (p-value = 0.006 via Chi-squared test) (Figure 1), and blood type A exhibited elevated levels of IL-6 (>35 pg/mL) in comparison to type B or O (p-value < 0.001 via Chi-squared test) (Figure 1). Figure 1 depicts the reduced usage of ventilators and lower mortality rates in patients with blood type O in comparison to those with other blood types.
There were no statistically significant differences between different ABO blood groups nor Rh factor in levels of other biomarkers of COVID-19 severity analyzed, which included the presence of abnormal monocytes, lymphocytes, megakaryocytes, and neutrophils on blood smear, percent and absolute neutrophil, monocyte, lymphocytes, eosinophils, basophils, D-dimers, CRP, hemoglobin, hematocrit, MCV, MCHC, RDW, platelets, AST, ALT, ALP, creatinine, creatinine kinase, PCT, PCT of 0.5–2.0 ng/mL, PCT > 2.0 ng/mL, hemoglobinuria, and hematuria.

3.2. Longitudinal Cohort Results: Cohort Characteristics

Among the participants included in this analysis (n = 185), 53% were healthcare workers, and 47% were at-risk community controls (Table 3) [29]. The median age was 51 ± 16.54, with 56.2% (104/185) female and 43.8% (81/185) male participants. Of all participants, 84.9% (157/185) identified as white and 63.2% (117/185) as non-Hispanic. There were 54% patients COVID-19 negative at baseline, whereas approximately 46% entered with a prior history of COVID-19. Including breakthrough or re-infection cases (95/185 (51.4%)), 76.2% (141/185) participants included in this analysis had experienced a positive COVID-19 test during their time on-study. Nearly all had been vaccinated (95.1% (176/185)), with most reporting primary vaccination with Pfizer-BioNTech (57.8% (107/185)), followed by Moderna (33% (61/185)), and Johnson & Johnson (4.3% (8/185)). Pfizer-BioNTech and Moderna COVID-19 vaccines were messenger RNA vaccines, whereas the Johnson & Johnson COVID-19 vaccine was a viral vector vaccine (Ad26.COV2-S recombinant). Eight participants (4.3%) were unvaccinated.

3.3. Longitudinal Cohort Results: ABO/Rh Blood Typing and COVID-19

Of our longitudinal cohort, approximately 47% (87/185) was ABO blood grouping type O, with 33.5% type A, and 14.1% and 5.4% B and AB, respectively. Additionally, 85.9% were Rh+. These observations were consistent across both sub-groups analyzed (HCW vs. CTL) (Table 4). As seen in Figure 2, we found no significant association between COVID status (infection vs. non-infection) and ABO (Chi-squared test [3, N = 185] = 1.8, p = 0.6) or Rh (Chi-squared test [1, N = 185] = 0.16, p = 0.7) blood typing.

4. Discussion

The results of our study highlighted a few concepts worth noting. Firstly, the ABO blood type distribution of our inpatient cohort was unique in that it varied from the normal general U.S. population distribution [30]. We also found that blood type O— was associated with decreased risk of both developing COVID-19 pneumonia and COVID-19-related mortality. Our data also illustrated that blood type O (Rh negative or positive) was associated with decreased elevations in troponin and LDH compared to accepted clinical baseline values. This finding may imply that patients with blood type O exhibited levels of biomarkers that indicated a diminished COVID-19 severity.
Prior immunological and microbiological research has found an association between blood type ABO and infection severity for SARS-CoV-1, Plasmodium falciparum, Helicobacter pylori, Norwalk virus, Hep B virus, and Neisseria gonorrhoeae [31]. Our finding that blood type O— demonstrated a decreased risk of developing COVID-19 and an associated decreased mortality has been corroborated by other studies [13,31,32,33,34,35,36,37,38,39]. The negative Rh factor of blood type O— may be a protective factor against severe COVID-19 illness [13,31], potentially making O— the most optimal blood type regarding protection against SARS-CoV-2 infection and severity in the scope of this study. It should be noted that adjusted p-values were not used in this study, as it was a hypothesis-generating exercise. All discovered associations warranted future investigation with a new cohort for confirmation.
Statistically significant differences were found in biomarkers of infection severity among blood types, which demonstrated that blood type O— had less elevated or more normal levels, such as those of LDH and troponin, which coincided with less severe infection. Elevated LDH and troponin levels have been correlated with severe COVID-19 [40], as is the case with such levels in the setting of infection from other pathogens. Interestingly, we also found that blood type O exhibited decreased levels of MCH, which may ultimately be due to decreased iron. A study by Hoque et al. comparing blood groups and serum iron levels noted that those with type O blood had the lowest hemoglobin and serum iron out of all the blood types, whereas type A donors had the highest mean TIBC levels [41]. RNA viruses require iron to replicate; thus, a depletion of iron may provide some viral mitigation [42]. Blood type A exhibited elevated levels of IL-6 (>35 pg/mL) in comparison to type B or O (p-value < 0.001 via Chi-squared test). Other studies have also shown variations in acute phase reactants (IL-6, CRP, Procalcitonin, and D-dimers) between the ABO blood types [17].
Some studies found that patients with blood type A had a higher risk of infection or severity than did those with type O [12,35,43]. The seemingly protective nature of blood type O against COVID-19 has been attributed to anti-A antibodies’ antagonization of SARS-CoV-2 and ACE-2 receptor bindings [11,43,44]. We question solely attributing this protective quality to one underlying mechanism, as our results demonstrated that specifically blood type O, but not B, was protective against COVID-19. Both blood type O and B have anti-A antibodies. Additionally, this hypothesis only accounts for S1B, not S1A, of the dual subunits of the SARS-CoV-2 monomer.
We posit an alternative theory, a theoretical–speculative concept that aligns with our study results and encompasses both potential binding sites of the virus. A higher amount of SARS-CoV-2 viral entry has been shown to coincide with a higher SARS-CoV-2 viral load with prolonged and more systemically dispersed viral shedding, which corresponds to greater COVID-19 severity [45,46]. Patients with mild cases of COVID-19 have demonstrated lower viral loads with a shorter duration of shedding that was more localized to their respiratory tract as compared to patients with severe cases [45]. Therefore, more viral entry may be associated with more severe COVID-19. Given this observed trend, the protective nature of blood type O against COVID-19 severity may be attributed to the diminished (5-N-acetyl-9-O-acetyl-) sialoside cluster formation through cis carbohydrate-carbohydrate stimulation, which may minimize the interaction of host cells with SARS-CoV-2 [47]. This mechanism can decrease the potential likelihood of binding of the N-terminal region of the polypeptide chain and receptor binding domains of the SARS-CoV-2 virus to CD147 and ACE2 receptors [47]. In short, blood type O may be protective against severe COVID-19 due to decreased sialoside expression, minimizing binding of SARS-CoV-2 virus to entry points on human cells. This notion is merely our speculation; further investigation into the underlying mechanism of the protective nature of blood type O against severe COVID-19 is warranted.
The lack of association between blood type and COVID-19 in our longitudinal cohort may be accounted for by mild cases that did not necessitate inpatient care. The discrepancy between statistically significant differences in findings in the inpatient, but not in the longitudinal, setting speaks to blood type ABO playing more of a role in overall severity of infection rather than in infectivity itself. We encourage further research into generalizable, global associations between blood type ABO and SARS-CoV-2 infection and severity.
Lastly, it is important to note that during the majority of the inpatient retrospective chart review investigation, COVID-19 vaccines were not yet developed. Our chart review spanned from 1 January 2020 to 31 March 2021. On 11 December 2020, the United States Food and Drug Administration issued the first emergency use authorization for the use of the Pfizer-BioNTech COVID-19 vaccine in persons aged 16 years and older [48]. Regarding our longitudinal cohort, most patients received the Pfizer-BioNTech COVID-19 vaccine (57.8%), then Moderna (33%), and, lastly, Johnson & Johnson (4.3%). Vaccines by Pfizer-BioNTech and Moderna have been touted to be the most effective in preventing severe infection via formation of antibodies and immunity [49]. Both vaccines can cause adverse effects, but these reactions are reported to be less frequent in patients administered Pfizer-BioNTech than Moderna [49]. However, a cited benefit of the Moderna vaccine is that it can be easily transported and stored because it is less temperature sensitive than the Pfizer-BioNTech vaccine [49]. Several cases of thromboses and Guillain–Barré syndrome due to the Johnson & Johnson vaccine were announced over the course of public administration, which spread hesitancy and reluctance in getting this manufacturer’s vaccine [50]. These trends were reflected by the vaccination status and distribution of our longitudinal cohort. Regardless of vaccination status, association of ABO blood type and COVID-19 was not statistically significant in this analyzed population.

Limitations

Our study was limited in external validity and, therefore, lacks generalizability to a larger population. This lack of generalizability was, in part, due to the demographic makeup of our South Florida population. Our population consists of a larger number of patients of Hispanic origin than does the general U.S. population. Additionally, generalizability is lacking in that selection bias is inherent within our inclusion criteria. Our inpatient cohort only included patients that presented to the emergency department, whereas the longitudinal cohort consisted solely of those presenting to the clinic that were willing to participate in a survey. Additionally, the selection process excluded the many COVID-19 positive patients that were asymptomatic as well as those that did not seek any professional medical care. There were many individuals infected with COVID-19 who were asymptomatic or had mild illnesses that, if included in this study, might have altered the results of the statistical analyses. Thus, our results must be properly applied to the inpatient and outpatient setting separately. The power of our study was limited due to our small sample sizes of 669 inpatient and 185 longitudinal participants. Lastly, our study contained limitations inherent to retrospective design, such as potential for residual confounding, incomplete or inaccurate chart data, or misclassification of exposures/outcomes.

5. Conclusions

Blood type appears to be associated with COVID-19 severity and mortality in inpatient populations. In an inpatient setting, blood type O sustained less risk of COVID-19 mortality, and blood type O— demonstrated less risk of developing COVID-19 pneumonia. In a longitudinal setting, there was no association found between blood type and COVID-19. As the novelty of COVID-19 declines with time, further studies on risk stratification by blood type are necessary to substantially establish an associative or causal relationship between the two. Future research studies regarding detailed clinical correlations and biomarker molecular mechanisms may shed light on how biomarker levels directly contribute to infection severity and clinical outcomes. We also encourage further research studies investigating the biomechanisms underlying the possible protectivity of blood type O against COVID-19 severity and mortality.

Author Contributions

All authors meet the four criteria for ICMJE authorship, which include (1) substantial contributions to the conception or design of the work, or the acquisition, analysis, or interpretation of data for the work, (2) drafting the work or revising it critically for important intellectual content, (3) final approval of the version to be published, and (4) agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. Conceptualization, T.E.; Data curation, T.E., C.J.C., N.P., Z.J.C., A.H., M.C., N.G., A.L., R.L., S.L., A.P., Y.A. and S.P. (Pahwa Savita); Formal analysis, T.E., A.M.A.M. and E.W.; Funding acquisition, S.P. (Pallikkuth Suresh) and S.P. (Pahwa Savita); Investigation, T.E., E.W., C.J.C., N.P., Z.J.C., A.H., M.C., N.G., A.L., R.L., A.P., Y.A., S.P. (Pallikkuth Suresh) and S.P. (Pahwa Savita); Methodology, T.E., A.M.A.M., E.W., S.P. (Pallikkuth Suresh) and S.P. (Pahwa Savita); Project administration, T.E. and S.P. (Pahwa Savita); Resources, T.E., S.L., S.P. (Pallikkuth Suresh) and S.P. (Pahwa Savita); Software, A.M.A.M. and E.W.; Supervision, T.E., and S.P. (Pahwa Savita); Validation, A.M.A.M., E.W. and S.P. (Pahwa Savita); Visualization, T.E.; Writing—original draft, T.E.; Writing—review and editing, T.E., A.M.A.M., E.W., C.J.C., N.P., Z.J.C., A.H., M.C., N.G., A.L., R.L., S.L., A.P., Y.A., S.P. (Pallikkuth Suresh) and S.P. (Pahwa Savita). All authors have read and agreed to the published version of the manuscript.

Funding

The retrospective chart review received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. The longitudinal prospective portion of this study is part of the PARIS /SPARTA studies funded by the NIAID Collaborative Influenza Vaccine Innovation Centers (CIVIC) contract 75N93019C00051 (PI F Krammer) with SGP as PI of the University of Miami site. Also supported by Miami Center for AIDS Research (CFAR) laboratory sciences core at the University of Miami Miller School of Medicine funded by a grant (P30AI073961) to SP from the NIH, which is supported by the following NIH Co-Funding and Participating Institutes and Centers: NIAID, NCI, NICHD, NHLBI, NIDA, NIMH, NIA, NIDDK, NIGMS, FIC, and OAR.

Institutional Review Board Statement

IRB approved (IRB: #20210025 and 20201026).

Informed Consent Statement

Patient consent obtained for the CITY longitudinal cohort study.

Data Availability Statement

The data that support the findings of this study are openly available at https://pubmed.ncbi.nlm.nih.gov and https://www.scopus.com/home.uri accessed on 1 January 2020 through July 2023.

Conflicts of Interest

The following authors have no financial disclosures or personal conflicts of interest: T.E., A.M.A.M., E.W., C.J.C., N.P., Z.J.C., A.H., M.C., N.G., A.L., R.L., S.L., A.P., Y.A., S.P. (Suresh Pallikkuth), and S.P. (Savita Pahwa).

Abbreviations

SARS-CoV-2—severe acute respiratory syndrome coronavirus-2; ED—emergency department; ARDS—diagnosis of acute respiratory distress syndrome; and Rh—rhesus.

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Figure 1. Presence (%) of COVID-19 findings in inpatient study cohort by blood type.
Figure 1. Presence (%) of COVID-19 findings in inpatient study cohort by blood type.
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Figure 2. ABO (A) and Rh (B).blood grouping in longitudinal CITY cohort by HCW and CTRL groups.
Figure 2. ABO (A) and Rh (B).blood grouping in longitudinal CITY cohort by HCW and CTRL groups.
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Table 1. Blood type distribution of the inpatient study cohort vs. general U.S. population.
Table 1. Blood type distribution of the inpatient study cohort vs. general U.S. population.
Blood TypeOverall Inpatient Study Cohort DistributionFemale Inpatient Study Cohort Distribution Male Inpatient Study Cohort DistributionRh PositiveRh Negative
O52.6% (n = 352)52.6% (n = 185) 47.4% (n = 167)86.6% (n = 305)13.4% (n = 47)
A35.3% (n = 236)50.8% (n = 120)49.2% (n = 116)88.6% (n = 209)11.4% (n = 27)
B10.8% (n = 72)51.4% (n = 37)48.6% (n = 35)100% (n = 72)0% (n = 0)
AB1.3% (n = 9)66.7% (n = 6)33.3% (n = 3)100% (n = 9)0% (n = 0)
Table 2. Distribution of conditions per blood type in inpatient study cohort.
Table 2. Distribution of conditions per blood type in inpatient study cohort.
ConditionA−A+AB+B+O−O+p-Value
COVID-19 pneumonia (n = 642)69.2%56.5%71.4%53.7%26.7%51.5%0.003
Elevated levels of LDH
(n = 376)		93.3%91.5%100%95.1%54.2%85.0%0.001
Normal levels of troponin (n = 389) 82.4%79.8%N/A95.6%66.7%83.8%0.026
AABBO
Mortality due to COVID-19 (n = 669)26.3%N/A29.2%17.0% 0.012
Decreased levels of MCH (n = 564)18.4%14.3%13.1%27.0% 0.006
Elevated levels of IL-6 > 35 pg/mL (n = 110)77.1%N/A20.0%47.1% <0.001
N/A—not available.
Table 3. Longitudinal CITY cohort characteristics.
Table 3. Longitudinal CITY cohort characteristics.
Frequency (%)
N185
Group
HCW98 (53%)
CTL87 (47%)
Age (Median ± SD; Range)51 ± 16.54; 20–93
Sex
Male81 (43.8%)
Female104 (56.2%)
Race
White157 (84.9%)
Asian11 (5.9%)
Black/African American10 (5.4%)
Other7 (3.8%)
Ethnicity
Hispanic117 (63.2%)
Not Hispanic68 (36.8%)
COVID-19 Vaccination Status
Vaccinated176 (95.1%)
Unvaccinated9 (4.9%)
Primary Vaccination
Pfizer-BioNTech (mRNA)107 (57.8%)
Moderna (mRNA)61 (33.0%)
Unvaccinated9 (4.9%)
Johnson & Johnson (viral vector)8 (4.3%)
Booster Vaccination132 (71.4%)
Pfizer-BioNTech (mRNA)77 (41.6%)
Moderna (half) (mRNA)34 (18.4%)
Moderna (full) (mRNA)21 (11.4%)
Table 4. COVID-19 status by ABO blood grouping in longitudinal CITY cohort.
Table 4. COVID-19 status by ABO blood grouping in longitudinal CITY cohort.
GroupCOVID PositiveCOVID NegativeTotal
(N = 185)
HCW 98 (53%)
   A19 (65.5%)10 (34.5%)29
   AB7 (100%)0 (0%)7
   B12 (70.6%)5 (29.5%)17
   O25 (61.0%)16 (39.0%)41
Rh+55 (67.1%)27 (32.0%)82
Rh−8 (66.7%)4 (33.3%)12
CTL 87 (47%)
   A28 (84.8%)5 (15.2%)33
   AB2 (66.7%)1 (33.3%)3
   B6 (66.7%)4 (8.7%)9
   O42 (91.3%)10 (34.5%)46
Rh+67 (87.0%)10 (13.0%)77
Rh−11 (78.6%)3 (21.4%)14
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Eatz, T.; Mantero, A.M.A.; Williams, E.; Cash, C.J.; Perez, N.; Cromar, Z.J.; Hernandez, A.; Cordova, M.; Godbole, N.; Le, A.; et al. Association of ABO Blood Type with Infection and Severity of COVID-19 in Inpatient and Longitudinal Cohorts. COVID 2023, 3, 1429-1439. https://doi.org/10.3390/covid3090098

AMA Style

Eatz T, Mantero AMA, Williams E, Cash CJ, Perez N, Cromar ZJ, Hernandez A, Cordova M, Godbole N, Le A, et al. Association of ABO Blood Type with Infection and Severity of COVID-19 in Inpatient and Longitudinal Cohorts. COVID. 2023; 3(9):1429-1439. https://doi.org/10.3390/covid3090098

Chicago/Turabian Style

Eatz, Tiffany, Alejandro Max Antonio Mantero, Erin Williams, Charles J. Cash, Nathalie Perez, Zachary J. Cromar, Adiel Hernandez, Matthew Cordova, Neha Godbole, Anh Le, and et al. 2023. "Association of ABO Blood Type with Infection and Severity of COVID-19 in Inpatient and Longitudinal Cohorts" COVID 3, no. 9: 1429-1439. https://doi.org/10.3390/covid3090098

APA Style

Eatz, T., Mantero, A. M. A., Williams, E., Cash, C. J., Perez, N., Cromar, Z. J., Hernandez, A., Cordova, M., Godbole, N., Le, A., Lin, R., Luo, S., Patel, A., Abu, Y., Pallikkuth, S., & Pahwa, S. (2023). Association of ABO Blood Type with Infection and Severity of COVID-19 in Inpatient and Longitudinal Cohorts. COVID, 3(9), 1429-1439. https://doi.org/10.3390/covid3090098

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