ABO and RhD blood group frequencies by race.

Naturally occurring antibodies against ABO antigens present in human sera have been shown to neutralize ABO-expressing HIV in vitro. We investigated associations between ABO and RhD blood groups and HIV infection among blood donors from all blood collection centers in eight of South Africa’s nine provinces. Whole blood donations collected from first time donors between January 2012 and September 2016 were tested for HIV RNA by nucleic acid testing and HIV antibody using third generation serology assays. ABO and RhD blood types were determined using automated technology. Odds ratios for the association between HIV positivity and ABO and RhD phenotypes were calculated using multivariable logistic regression analysis. We analyzed 515,945 first time blood donors and the overall HIV prevalence was 1.12% (n = 5790). After multivariable adjustment, HIV infection was weakly associated with RhD positive phenotype (OR = 1.15, 95% CI 1.00–1.33) but not with ABO blood group. The observed association with RhD positive phenotype was marginal and likely due to residual confounding by racial group but could serve to generate hypotheses for further studies.</div

Demographic characteristics and multivariable analysis of 515 397 first time donors between January 2012 and December 2016 showing the effect of donor demographics and ABO and RhD blood group on HIV positive status.

Demographic characteristics and multivariable analysis of 515 397 first time donors between January 2012 and December 2016 showing the effect of donor demographics and ABO and RhD blood group on HIV positive status.</p

HIV Infectivity of PBMCs from SCD Patients and non-SCD Controls.

CD8-depleted PBMC from SCD patients and non-SCD controls were infected with HIV NL4-3 (CXCR4-tropic) and 81-A (CCR5-tropic) at increasing MOI for six days. Following incubation, supernatants and cells were harvested for detection of HIV p24 (Panel A) and pro-viral load (Panel B) respectively. Mean and standard errors of the means for 30 SCD patients and 30 non-SCD controls are shown. Samples from four SCD patients and two non-SCD controls spanning a range of proviral load were assayed for integrated HIV DNA (Panel C). Five samples showed undetectable HIV DNA on both assays and are not graphed. The linear regression line of the log10 values is shown.</p

Comparison of HIV co-receptors, CD4+ T cell activation markers, CD4+ MFI and Percent of CD4+ Cells Among Total T Cells between SCD patients and non-SCD controls.

Twenty four-hour old whole blood samples from SCD patient and non-SCD controls were labeled for CD4 T cells and incubated with antibodies to detect markers associated with HIV or cellular activation. Following incubation, surface expression of the HIV co-receptors CCR5 and CXCR4 and T cell trafficking molecule CCR7 were measured by flow cytometry (Panel A). MFI, mean fluorescence intensity between SCD patients and non-SCD controls were compared. Percent of CD4+ T cells expressing the activation markers CD38 or HLA-DR were measured and compared between SCD patients and non-SCD controls (Panel B). The intensity of expression of CD4+ amongst T cells (Panel C) and the percent of CD4+ T cells among total T cells (Panel D) was significantly higher in SCD patients compared to non-SCD controls. Mean and standard errors of the means for 30 SCD patients and 30 non-SCD controls are shown, *p<0.05.</p

Baseline characteristics of participants in the transfusion safety study at study entry, by HIV status.

Baseline characteristics of participants in the transfusion safety study at study entry, by HIV status.</p

Cytokines and Chemokines Compared between SCD Patients (treated or not treated with HU) and non-SCD Controls.

Biomarkers tested are grouped into anti-inflammatory (AI), chemoattractant (CA), coagulation (CO), growth factor (GF) and pro-inflammatory (PI) functional categories. Relative increases in concentration are shown in red and decreases in blue. * significantly different between SCD patients and non-SCD controls (p<0.05 after FDR correction).</p

Odds of HIV Acquisition in TSS.

Odds of HIV Acquisition in TSS.</p

Demographics of 30 SCD Subjects Prospectively Enrolled to Investigate Mechanisms of Resistance to HIV.

Demographics of 30 SCD Subjects Prospectively Enrolled to Investigate Mechanisms of Resistance to HIV.</p

HIV Infectivity of Target MT-2 cells in the Presence of Plasma from SCD Patients or Plasma from Non-SCD Controls.

MT-2 cells maintained at log phase growth were infected with either HIV NL4-3 (Panel A) or 81-A virus (Panel B) at MOI of 10−2 in cultures spiked with 20% plasma from SCD patients or non-SCD controls. Following 7-day infections supernatants were measured for p24 by ELISA. Mean and SEM are shown. * p<0.05.</p

Hb S/<b>β</b>-Thalassemia in the REDS-III Brazil Sickle Cell Disease Cohort: Clinical, Laboratory and Molecular Characteristics

We described the clinical, laboratory and molecular characteristics of individuals with Hb S (HBB: c.20A>T)/β-thalassemia (Hb S/β-thal) participating in the Recipient Epidemiology and Donor Evaluation Study (REDS-III) Brazil Sickle Cell Disease cohort. HBB gene sequencing was performed to genotype each β-thal mutation. Patients were classified as Hb S/β0-thal, Hb S/β+-thal-severe or Hb S/β+-thal based on prior literature and databases of hemoglobin (Hb) variants. Characteristics of patients with each β-thal mutation were described and the clinical profile of patients grouped into Hb S/β0-thal, Hb S/β+-thal and Hb S/β+-thal-severe were compared. Of the 2793 patients enrolled, 84 (3.0%) had Hb S/β0-thal and 83 (3.0%) had Hb S/β+-thal; 40/83 (48.2%) patients with Hb S/β+-thal had mutations defined as severe. We identified 19 different β-thal mutations, eight Hb S/β0-thal, three Hb S/β+-thal-severe and eight Hb S/β+-thal. The most frequent β0 and β+ mutations were codon 39 (HBB: c.118C>T) and IVS-I-6 (T>C) (HBB: c.92+6T>C), respectively. Individuals with Hb S/β0-thal had a similar clinical and laboratory phenotype when compared to those with Hb S/β+-thal-severe. Individuals with Hb S/β+-thal-severe had significantly lower total Hb and Hb A levels and higher Hb S, white blood cell (WBC) count, platelets and hemolysis markers when compared to those with Hb S/β+-thal. Likewise, individuals with Hb S/β+-thal-severe showed a significantly higher occurrence of hospitalizations, vaso-occlusive events (VOE), acute chest syndrome (ACS), splenic sequestration, blood utilization, and hydroxyurea (HU) therapy.</p