Individuals with inherited immunodeficiencies, autoimmune disorders, organ or bone marrow transplantation, or infection with human immunodeficiency virus (HIV) are at increased risk of infection with both low-risk and high-risk human papillomavirus (HPV) types. Chronic immunosuppression provides an environment for persistent HPV infection which carries a higher risk of malignant transformation. Screening guidelines have been developed or advocated for processes that have detectable premalignant lesions, such as anal cancer or cervical cancer. For other anatomic locations, such as cutaneous, penile, and oropharyngeal, a biopsy of suspicious lesions is necessary for diagnosis. HPV cannot be cultured from clinical specimens in the laboratory, and diagnosis relies on cytologic, histologic, or molecular methods.

Transfusion of red blood cells (RBC) remains a primary treatment modality in patients with sickle cell disease (SCD). Repeated exposure to alloantigens on transfused RBCs can lead to alloantibody formation that can increase the risk of delayed hemolytic transfusion reaction (DHTR). 1 The incidence of DHTR in transfused adult SCD patients ranged from 4.8-7.7% during a 30-month and 5-year study period, respectively. 2,3 The case fatality rate is 6%. 4 The symptoms of DHTR typically appear 7-14 days post-transfusion and include generalized pain, hemoglobinuria with/without fever, a significant drop of total hemoglobin and hemoglobin A from the post-transfusion value and suboptimal reticulocyte response. These clinical features mimic a classic vaso-occlusive pain crisis (VOC), further confounding the detection of DHTR. In addition, patients can experience hyperhemolysis, evidenced by hemolysis of both native and transfused RBCs. General management of DHTR depends on the extent of hemolysis and the patient's clinical condition, from supportive care strategies to high dose erythropoietin, intravenous immunoglobulin (IVIg), and immunosuppression. 4,5 We report here comprehensive data on a 14-year-old African American female with SCD (β s β s genotype) and evidence for alternative complement pathway (ACP) activation during two of her three DHTR hyperhemolysis episodes, one of which had no new detectable allo-or autoantibody. This patient's past medical history is significant for multiple episodes of acute chest syndrome (ACS) and VOC, and an episode of acute splenic seques-

BACKGROUND: In 2014, passive immunization by transfusion of Ebola convalescent plasma (ECP) was considered for treating patients with acute Ebola virus disease (EVD). Early Ebola virus (EBOV) seroconversion confers a survival advantage in natural infection, hence transfusion of ECP plasma with high levels of neutralizing EBOV antibodies is a potential passive immune therapy. Techniques to reduce the risk of other transfusion-transmitted infections (TTIs) are warranted as recent ECP survivors are ineligible as routine blood donors. As part of an ongoing clinical trial to evaluate the safety and effectiveness of ECP, the impact of amotosalen/UVA pathogen reduction technology (PRT) on EBOV antibody characteristics was examined.STUDY DESIGN AND METHODS: Serum and plasma samples were collected from EVD-recovered subjects at multiple timepoints and evaluated by ELISA for antibodies to recombinant EBOV glycoprotein (GP) and irradiated whole EBOV antigen, as well as for EBOV microneutralization, classic plaque reduction neutralization test (PRNT) and EBOV pseudovirion neutralization assay (PsVNA) activity. RESULTS: Six subjects donated 40 individual ECPunits. Substantial antibody titers and neutralizing activity results were demonstrated but were generally lower for the ACD plasma samples compared to the serum samples. Anti-EBOV titers by all assays remained essentially unchanged after PRT.CONCLUSION: Treatment of ECP with PRT to reduce the risk of TTI did not significantly reduce EBOV IgG antibody titers or neutralizing activity. Although ECP was used in the treatment of repatriated patients, no PRT units from this study were transfused to EVD patients. This inventory of PRT-treated ECP is currently available for future clinical evaluation.From the

The mandated testing of blood components for infectious diseases, to prevent transfusion-transmitted infections (TTIs), began in the 1950s. Since then, changes in predonation questionnaires and advances in testing techniques have afforded more sensitive and specific tests for pathogens, in addition to allowing earlier detection. Given that these approaches have very low but detectable failure rates, the recent development and implementation of proactive pathogen reduction approaches is the new forefront of TTI prevention strategies. With globalization and the ability of pathogens to evolve rapidly, continuous redefining of testing standards and laboratory techniques is paramount for maintaining a safe blood supply.

BACKGROUND Delayed hemolytic transfusion reactions (DHTRs) are serious complications of RBC transfusion that can occur in previously alloimmunized patients. Patients who require episodic transfusions during heightened inflammatory states, such as patients with sickle cell disease (SCD), are particularly prone to alloimmunization and developing DHTRs with hyperhemolysis. While efforts to mitigate these hemolytic episodes via immunosuppressive drugs can be employed, the relative efficacy of various treatment options remains incompletely understood. CASE REPORTS In this study, we explored five patients with SCD and multiple RBC alloantibodies who received various forms of immunosuppressive therapy in an attempt to prevent or treat severe DHTRs. RESULTS The clinical course for these five patients provides insight into the difficulty of effectively treating and preventing DHTRs in patients with SCD with currently available immunosuppressive therapies. CONCLUSION Based on our experience, and the current literature, it is difficult to predict the potential impact of various immunosuppressive therapies when seeking to prevent or treat DHTRs. Future mechanistic studies are needed to identify the optimal treatment options for DHTRs in the presence or absence of distinct alloantibodies in patients with SCD.

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Previously, a distinct MHC class II Luminex-single antigen bead (SAB) pattern was described and attributed to antibodies targeting denatured antigens. In this study, we describe a distinct MHC class I reactivity pattern observed in 1.8% (105/5992) of samples resulted in 2017. The pattern displays reactivity to the following Luminex-

BACKGROUND: Hemolytic transfusion reactions are a rare, yet serious complication of red blood cell (RBC) transfusion. Patients with sickle cell disease (SCD) are at an increased risk for such reactions, because they are prone to make alloantibodies against transfused RBCs, complicating this integral part of their disease management. These reactions may be missed, and the patient's state may be attributed to vaso-occlusive crisis (VOC), with misguided therapy ensuing.CASE REPORT: Herein, we report the clinical course of a patient with complex SCD with a delayed hemolytic transfusion reaction, followed by multiple acute hemolytic transfusion reactions mistaken for severe VOC. These reactions were diagnosed on retrospective review of the patient's clinical course in consult with the transfusion medicine service. Optimal immunosuppressive therapy ensued and resulted in the stabilization of the anemia and hemolysis laboratory values. Despite these efforts, the patient died 2 months after admission. CONCLUSION:This case provides insight into some of the challenges of managing patients with SCD with multiple comorbidities. Hemolytic transfusion reactions can be difficult to diagnose and may be overlooked in patients with SCD with severe VOC. ABBREVIATIONS: AHTR = acute hemolytic transfusion reaction; ARC = absolute reticulocyte count; CAA = cold autoantibody; CHF = congestive heart failure; DAT = direct antiglobulin test; DHTR = delayed hemolytic transfusion reaction; DVT = deep venous thrombosis; Hb = hemoglobin; IAT = indirect antiglobulin test; IRL = immunohematology reference laboratory; LDH = lactate dehydrogenase; PEG = polyethylene glycol; RBC = red blood cell; SCD = sickle cell disease; TB = total bilirubin; VOC = vaso-occlusive crisis.