Human serum contains large amounts of anti-carbohydrate antibodies, some of which may recognize epitopes on viral glycans. Here, we tested the hypothesis that such antibodies may confer protection against COVID-19 so that patients would be preferentially found among people with low amounts of specific anti-carbohydrate antibodies since individual repertoires vary considerably. After selecting glycan epitopes commonly represented in the human anti-carbohydrate antibody repertoire that may also be expressed on viral glycans, plasma levels of the corresponding antibodies were determined by ELISA in 88 SARS-CoV-2 infected individuals, including 13 asymptomatic, and in 82 non-infected controls. We observed that anti-Tn antibodies levels were significantly lower in patients as compared to non-infected individuals. This was not observed for any of the other tested carbohydrate epitopes, including anti-αGal antibodies used as a negative control since the epitope cannot be synthesized by humans. Owing to structural homologies with blood groups A and B antigens, we also observed that anti-Tn and anti-αGal antibodies levels were lower in blood group A and B, respectively. Analyses of correlations between anti-Tn and the other anti-carbohydrates tested revealed divergent patterns of correlations between patients and controls, suggesting qualitative differences in addition to the quantitative difference. Furthermore, anti-Tn levels correlated with anti-S protein levels in the patients’ group, suggesting that anti-Tn might contribute to the development of the specific antiviral response. Overall, this first analysis allows to hypothesize that natural anti-Tn antibodies might be protective against COVID-19.
BackgroundRHCE*ceEK is a rare RH allele mostly encountered in people of African descent. This allele is defined by four single nucleotide substitutions: c.48G>C, c.712A>G, c.787A>G and c.800T>A. Until now, it has only been reported to segregate with either RHD*01N.01 or RHD*DAR1.00.Materials and MethodsBlood samples were drawn from a 32‐year‐old Tutsi pregnant woman during an antenatal visit in order to perform her type and screen. To further investigate the results found in the patient, a family study was conducted. Standard haemagglutination methods were used to investigate the subjects’ red blood cells and plasma. Molecular workup on RHD and RHCE genes was carried out by DNA microarray, real‐time PCR and DNA sequencing techniques.ResultsThe patient was phenotyped as group B, D+C−E−c+e+, Hr−. A complex mixture of anti‐E, anti‐c, anti‐Hr and anti‐hrS was detected in her plasma. She was found to carry a normal RHD gene, a conventional RHCE*ceEK allele and an alternative RHCE*ceEK allele (RHCE*ceEK without c.48G>C). The family study showed that the conventional RHCE*ceEK and the alternative RHCE*ceEK alleles were associated with a RHD*01 allele and a RHD*01N.01 allele, respectively. Molecular analysis performed in the proband’s mother showed a novel RHCE*ce variant allele on a RHCE*ceS‐like background (RHCE*ceS with c.609G>A).ConclusionsThis case study brought out new associations between RHD and RHCE alleles encoding the rare Hr− phenotype: the conventional RHCE*ceEK allele linked to the RHD*01 allele and an alternative RHCE*ceEK allele associated with the RHD*01N.01 allele. A novel RHCE*ce variant (RHCE*ceS with c.609G>A) was also reported.
BACKGROUND
Mta (MNS14) is a low‐prevalence antigen of the MNS system. A few cases of hemolytic disease of the fetus and newborn caused by anti‐Mta have been reported in the literature, but up to now this antibody has never been associated with a hemolytic transfusion reaction (HTR).
CASE REPORT
A 38‐year‐old male with sickle cell disease undergoing exchange transfusion presented with shivering, nausea, dyspnea, and pain in the lower limbs. Biologic parameters showed increased hemolysis. The administered red blood cell (RBC) units had been issued by electronic crossmatch due to a negative antibody screening test. In the posttransfusion investigations, crossmatch of the transfused RBC units with the patient's serum showed incompatibility of one unit. The presence of an antibody against a low‐prevalence antigen was suspected and further serologic testing was performed for identification.
RESULTS
Anti‐Mta was identified in the patient's serum. The RBCs of the incompatible unit implicated in the HTR were Mt(a+). An eluate of a posttransfusion blood sample of the patient was nonreactive with the incompatible RBCs, and the direct antiglobulin test was negative.
CONCLUSION
To our knowledge, this is the first case report of an HTR associated with anti‐Mta.
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