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BACKGROUND. Initial reports from the severe acute respiratory coronavirus 2 (SARS-CoV-2) pandemic described children as being less susceptible to coronavirus disease 2019 (COVID-19) than adults. Subsequently, a severe and novel pediatric disorder termed multisystem inflammatory syndrome in children (MIS-C) emerged. We report on unique hematologic and immunologic parameters that distinguish between COVID-19 and MIS-C and provide insight into pathophysiology. METHODS. We prospectively enrolled hospitalized patients with evidence of SARS-CoV-2 infection and classified them as having MIS-C or COVID-19. Patients with COVID-19 were classified as having either minimal or severe disease. Cytokine profiles, viral cycle thresholds (Cts), blood smears, and soluble C5b-9 values were analyzed with clinical data. RESULTS. Twenty patients were enrolled (9 severe COVID-19, 5 minimal COVID-19, and 6 MIS-C). Five cytokines (IFN- [gamma], IL-10, IL-6, IL-8, and TNF-[alpha]) contributed to the analysis. TNF-[alpha] and IL-10 discriminated between patients with MIS-C and severe COVID-19. The presence of burr cells on blood smears, as well as Cts, differentiated between patients with severe COVID-19 and those with MIS-C. CONCLUSION. Pediatric patients with SARS-CoV-2 are at risk for critical illness with severe COVID-19 and MIS-C. Cytokine profiling and examination of peripheral blood smears may distinguish between patients with MIS-C and those with severe COVID-19. FUNDING. Financial support for this project was provided by CHOP Frontiers Program Immune Dysregulation Team; National Institute of Allergy and Infectious Diseases; National Cancer Institute; the Leukemia and Lymphoma Society; Cookies for Kids Cancer; Alex's Lemonade Stand Foundation for Childhood Cancer; Children's Oncology Group; Stand UP 2 Cancer; Team Connor; the Kate Amato Foundations; Burroughs Wellcome Fund CAMS; the Clinical Immunology Society; the American Academy of Allergy, Asthma, and Immunology; and the Institute for Translational Medicine and Therapeutics., Introduction Initial reports from the coronavirus disease 2019 (COVID-19) pandemic indicated that children were less severely affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection than adults (1-3). The [...]

BACKGROUND. Pediatric SARS-CoV-2 infection can be complicated by a dangerous hyperinflammatory condition termed multisystem inflammatory syndrome in children (MIS-C). The clinical and immunologic spectrum of MIS-C and its relationship to other inflammatory conditions of childhood have not been studied in detail. METHODS. We retrospectively studied confirmed cases of MIS-C at our institution from March to June 2020. The clinical characteristics, laboratory studies, and treatment response were collected. Data were compared with historic cohorts of Kawasaki disease (KD) and macrophage activation syndrome (MAS). RESULTS. Twenty-eight patients fulfilled the case definition of MIS-C. Median age at presentation was 9 years (range: 1 month to 17 years); 50% of patients had preexisting conditions. All patients had laboratory confirmation of SARS- CoV-2 infection. Seventeen patients (61%) required intensive care, including 7 patients (25%) who required inotrope support. Seven patients (25%) met criteria for complete or incomplete KD, and coronary abnormalities were found in 6 cases. Lymphopenia, thrombocytopenia, and elevation in inflammatory markers, D-dimer, B-type natriuretic peptide, IL-6, and IL-10 levels were common but not ubiquitous. Cytopenias distinguished MIS-C from KD and the degree of hyperferritinemia and pattern of cytokine production differed between MIS-C and MAS. Immunomodulatory therapy given to patients with MIS-C included intravenous immune globulin (IVIG) (71%), corticosteroids (61%), and anakinra (18%). Clinical and laboratory improvement were observed in all cases, including 6 cases that did not require immunomodulatory therapy. No mortality was recorded in this cohort. CONCLUSION. MIS-C encompasses a broad phenotypic spectrum with clinical and laboratory features distinct from KD and MAS. FUNDING. This work was supported by the National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases; the National Institute of Allergy and Infectious Diseases; Rheumatology Research Foundation Investigator Awards and Medical Education Award; Boston Children's Hospital Faculty Career Development Awards; the McCance Family Foundation; and the Samara Jan Turkel Center., Introduction Since the onset of the Coronavirus disease 2019 (COVID-19) pandemic, millions of individuals have been infected with severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) and more than 500,000 deaths [...]

A 996 bp Aspergillus nidulans cDNA which encodes the ASPND1 immunodominant antigen was cloned and expressed in Escherichia coli as a fusion protein with the enzyme glutathione S-transferase (GST) from Schistoma japonicum. The GST-ASPND1 fusion protein was purified and after cleavage with thrombin, the ASPND1 recombinant antigen (ASPND1r) and the GST protein were separated and immunobloted with several human sera. The sera from 22 out of 25 patients with an aspergilloma recognized the ASPND1r recombinant antigen on immunoblots. Forty-nine normal human sera and 14 sera from patients with other infections were unreactive.

A monoclonal antibody (MAb) designated EM-7G1 was developed from a previously developed MAb which reacts to the 76-, 66-, 56- and 52-kDa antigens of Listeria monocytogenes. EM-7G1 reacts specifically to the 66-kDa antigen, and detected all strains of L. monocytogenes tested with no cross-reaction with other Listeria spp. Therefore,this MAb should be useful for detecting L. monocytogenes in food or clinical samples through enzyme-linked immunoassays or microcolony immunoblotting.

Monoclonal antibodies (mAbs) were raised against porin proteins of encapsulated and unencapsulated strains of Haemophilus influenzae. Three mAbs, P2-17, P2-18 and P2-19 were found to react with the epitopes of both types of strains. P2-18 reacted to P2 epitopes common to all strains of the pathogen while P2-17 and P2-19 mAbs failed to react with epitopes in 70-100% of the strains screened. The domain of the P2-specific epitope was within the N-terminal region (residues 1 to 14), while the P2-17 and P2-19-specific epitopes were localized between residues 28 and 55, and 101 and 129, respectively.