Background: Coronavirus disease 2019 (COVID-19) convalescent plasma (CCP) collection began in two Brazilian hospitals for treatment of severe/ critical patients. Methods and Materials: Mild/moderate COVID-19 convalescents were selected as CCP donors after reverse transcription polymerase chain reaction (RT-PCR) confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and absence of symptoms for ≥14 days plus (a) age (18-60 years), body weight greater than 55 kg; (b) immunohematological studies; (c) no infectious markers of hepatitis B virus, hepatitis C virus, human immunodeficiency virus, human T-lymphotropic virus-1/2, Chagas and syphilis infection; (d) no HLA antibodies (multiparous); (e) second RT-PCR (nasopharyngeal swab and/or blood) negativity; (f) virus neutralization test (cytopathic effect-based virus neutralization test neutralizing antibody) and anti-nucleocapsid protein SARS-CoV-2 IgM, IgG, and IgA enzyme-linked immunosorbent assays. Results: Among 271 donors (41 females, 230 males), 250 presented with neutralizing antibodies. Final RT-PCR was negative on swab (77.0%) or blood (88.4%; P = .46). Final definition of RT-PCR was only defined at more than 28 days after full recovery in 59 of 174 (33.9%) RT-PCR-ve, and 25/69 RT-PCR +ve (36.2%;

The formula of Pierelli et al. is associated with a PPV that is high, moderate, and relatively low for the corresponding predicted CD34+ doses.

Background RHD alleles leading to a reduced expression of D antigen of the red blood cell (RBC) surface may be erroneously typed as D− by serology and may cause anti‐D immunizations when transfused to recipients. Methods To determine the occurrence of such alleles among apparent D− blood donors, molecular typing was implemented as a routine test using a pool of DNA. A total of 2,450 pretyped D− samples were tested in pools of 10 for the RHD‐specific polymorphism in intron 4 and exon 7. Samples in polymer chain reaction (PCR) positive pools were individually reevaluated by exon‐specific PCRs, sequencing, and serologic methods. Results Among 2,450 serologically D− blood donor samples tested, 101 (4.1%) carried the RHD gene. Nonfunctional RHD (RHDψ, RHD*CE(2–9)‐D, and RHD*CE(3–7)‐D), different weak D alleles such as RHD*weak D type 1, RHD*weak D type 4.3, RHD*weak D type 5, RHD*weak D type 38, and RHD*DEL were identified. Conclusion We employed a PCR‐based assay for RHD as a routine test using pools of ten DNA blood donor samples. The integration of RHD genotyping into the routine screening program using pools of DNA samples was straightforward. As a consequence, 19 (0.8%) blood donors carrying a weak D and Del phenotypes with the potential of causing anti‐D immunizations in recipients were reclassified as D+. For each population, it would be necessary to adapt the RHD genotyping strategy to the spectrum of prevalent alleles.

Background Blood groups and anti‐A isohemagglutinin may be involved in susceptibility to SARS‐CoV‐2 infection. Materials and Methods We retrospectively studied 268 COVID‐19 convalescent plasma donors and 162 COVID‐19 inpatients (total 430 subjects, confirmed by RT‐PCR) and 2,212 healthy volunteer first‐time blood donors as a control group. These were further divided into two groups: those with anti‐A (blood types O and B) and those without it (types A and AB). Titres of nucleoproteins, and neutralizing SARS‐CoV‐2 antibody were measured in the convalescent plasma donors and inpatients. Multivariate logistic regression and non‐parametric tests were applied. Results Persons having types O or B showed less infection prevalence than those of types A or AB (OR = 0·62, 95% CI 0·50–0·78; P < 0·001), but there was no difference when COVID‐19 inpatients were analysed. Immunoglobulins M, G and A were lower in COVID‐19 subjects of types O or B group than those of A or AB (0·16 vs. 0·19; P = 0·03, 2·11 vs. 2·55; P = 0·02, 0·23 vs. 0·32; P = 0·03, respectively). Conclusion In this retrospective cohort, COVID‐19 individuals were less likely to belong to blood types O and B, and also had lower SARS‐CoV‐2 antibody titres than A and AB individuals. COVID‐19 severity did not associate with the blood groups.