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BACKGROUND: Five cases of transfusion transmission of hepatitis E virus (HEV) have been reported so far. The infection routes of the causative donors remain unclear, however. Also, the progress of virus markers in the entire course of HEV infection has not been well documented. STUDY DESIGN AND METHODS: Nucleic acid testing was performed by real-time reverse transcription–polymerase chain reaction targeting the open reading frame 2 region of HEV. Full-length nucleotide sequences of HEV RNA were detected by direct sequencing. RESULTS: Lookback study of a HEV-positive donor revealed that the platelets (PLTs) donated from him 2 weeks previously contained HEV RNA and were transfused to a patient. Thirteen relatives including the donor were ascertained to enjoy grilled pork meats together in a barbecue restaurant 23 days before the donation. Thereafter, his father died of fulminant hepatitis E and the other 6 members showed serum markers of HEV infection. In the recipient, HEV was detected in serum on Day 22 and reached the peak of 7.2 log copies per mL on Day 44 followed by the steep increase of alanine aminotransferase. Immunoglobulin G anti-HEV emerged on Day 67; subsequently, hepatitis was resolved. HEV RNA sequences from the donor and recipient were an identical, Japan-indigenous strain of genotype 4. HEV RNA was detectable up to Day 97 in serum, Day 85 in feces, and Day 71 in saliva. CONCLUSION: A transfusion-transmitted hepatitis E case by blood from a donor infected via the zoonotic food-borne route and the progress of HEV markers in the entire course are demonstrated. Further studies are needed to clarify the epidemiology and the transfusion-related risks for HEV even in industrialized countries. [ABSTRACT FROM AUTHOR]

BACKGROUND: HLA Class II antibodies are thought to be involved in severe transfusion reactions including transfusion-related acute lung injury (TRALI). The activation of monocytes by HLA Class II antibody may play an important role in the etiology of TRALI. CASE REPORT: An 81-year-old man with non-Hodgkin's lymphoma (Clinical Stage IIIA) received a plateletpheresis unit containing at least 4 × 1011 platelets because of thrombocytopenia and a bleeding tendency. Approximately 30 minutes after the start of transfusion, he developed chills, tachycardia, dyspnea, lumber, and abdominal pain and then a fever (40.3°C). His SaO2 dropped to 70 percent. The transfusion was discontinued immediately. His symptoms disappeared after treatment with oxygen and the administration of corticosteroid and aminophyrine. A chest X-ray showed no sign of pulmonary edema. RESULTS: The donor serum sample had HLA-DR antibodies against multiple DR antigens including DR13, the recipient's HLA-DR type. The cross-match between the patient's lymphocytes and the donor serum was positive. The treatment of peripheral blood mononuclear cells from healthy subjects bearing DR13 antigen with the donor plasma caused the secretion of inflammatory cytokines (i.e., interleukin [IL]-1β, IL-6, and tumor necrosis factor-α) and neutrophil-activating chemokines (i.e., IL-8 and CXCL1/GRO-α) in a cognate antigen-antibody relationship. In addition, the secretion of inflammatory cytokines appeared to require the involvement of CD32 and/or CD16. CONCLUSION: HLA-DR antibodies, detected in this case, had biologic functions to induce production of not only inflammatory cytokines but also neutrophil-attractant chemokines in vitro, which could contribute to the etiology of severe nonhemolytic transfusion reactions. [ABSTRACT FROM AUTHOR]

In industrialized countries, sporadic cases of hepatitis E have been reported in individuals who have never been in an endemic area. Hepatitis E virus (HEV) infection commonly occurs via the fecal-oral route but a potential risk of transfusion transmission route has been suggested. A 67-year-old Japanese male patient who had never been abroad received a transfusion of blood from 23 voluntary donors and developed acute hepatitis with unknown etiology after transfusion. His blood samples were tested for viral markers of hepatitis viruses. HAV, HBV, HCV, CMV, and EBV were ruled out as causative agents in this case. The patient's blood sample in the acute phase contained HEV RNA as well as IgM and IgG anti-HEV. HEV RNA was also detected in one of the FFP units transfused. The donor had no history of traveling abroad and had a normal ALT level at the time of donation. The PCR products from the patient and the donor showed complete identity for two distinct regions of HEV within open reading frame 1. The patient was infected with HEV via transfused blood from a volunteer donor. A potential risk of posttransfusion hepatitis E should be considered even in nonendemic countries. [ABSTRACT FROM AUTHOR]

Background: RANTES, one of the PLT-derived biologic response modifiers, accumulates in PLT concentrates (PCs) during storage and may play a causative role in nonhemolytic transfusion reactions (NHTRs) after PC transfusion.Study Design and Methods: To investigate the association of RANTES with NHTRs, the biologic activity of RANTES in the supernatant of stored PC at the intravascular concentration expected after PC transfusion was assessed by examining chemotaxis and histamine release in human basophils. In addition, the levels of RANTES in PCs involved in NHTRs were compared with those in PCs causing no transfusion reactions.Results: The supernatant of PC diluted to contain 1 nM RANTES significantly increased the migration of and release of histamine from basophils. Neutralizing antibody to RANTES suppressed the PC-triggered migration, but not histamine release. The levels of RANTES in PCs involved in NHTRs after PC transfusion were comparable to those in PCs that did not cause any transfusion reactions.Conclusion: RANTES that accumulated in PCs during storage was biologically active in a basophil chemotaxis assay at the intravascular concentration expected after PC transfusion. However, the NHTRs after PC transfusion were not simply related to the RANTES level in PCs. [ABSTRACT FROM AUTHOR]