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1. Prior infection by seasonal coronaviruses, as assessed by serology, does not prevent SARS-CoV-2 infection and disease in children, France, April to June 2020

Author

Marina Charbit, Johanne Auriau, Dulanjalee Kariyawasam, Isabelle Sermet-Gaudelus, Marc Eloit, Elsa Foucaud, Christèle Huon, Albert Faye, Delphine Chrétien, Flora Donati, Tiffany Guilleminot, Vincent Enouf, Bettina Mesplees, Coralie Briand, Marianne Leruez-Ville, Mélodie Aubart, Thomas Bigot, Sylvie van der Werf, Sarah Temmam, Brigitte Bader-Meunier, Mélanie Albert, Célia Crétolle, Agnès Delaunay-Moisan, Gilles Orliaguet, Grégoire Benoist, Vincent Gajdos, L. Fertitta, Bénédicte Pigneur, Julie Toubiana, Thibaut Lurier, Sylvie Behillil, Marija Backovic, Mathie Lorrot, marc duval-arnould, Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Université Paris Cité - UFR Médecine [Santé] (UPCité UFR Médecine), Université Paris Cité (UPCité), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Découverte de pathogènes – Pathogen discovery, Institut Pasteur [Paris] (IP), Centre National de Référence des virus des infections respiratoires (dont la grippe) - National Reference Center Virus Influenzae [Paris] (CNR), Génétique Moléculaire des Virus à ARN - Molecular Genetics of RNA Viruses (GMV-ARN (UMR_3569 / U-Pasteur_2)), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), AP-HP - Hôpital Antoine Béclère [Clamart], Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche d'Épidémiologie des maladies Animales et zoonotiques (UMR EPIA), VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Rongeurs Sauvages, Risques Sanitaires et Gestion des Populations - UR 1233 (RS2GP), Virologie Structurale - Structural Virology, Département Plateforme (PF I2BC), Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Hôpital Jean Verdier [AP-HP], Hôpital Louis Mourier - AP-HP [Colombes], Hôpital Ambroise Paré [AP-HP], Hôpital Robert Debré Paris, Hôpital Robert Debré, AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Plateforme de Microbiologie Mutualisée (PIBnet) - Mutualized Platform for Microbiology (P2M), Pasteur International Bioresources network (PIBNet), Biodiversité et Epidémiologie des Bactéries pathogènes - Biodiversity and Epidemiology of Bacterial Pathogens, Laboratoire de Microbiologie Clinique [AP-HP Hôpital Necker-Enfants Malades], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), École nationale vétérinaire - Alfort (ENVA), This work was supported by the « URGENCE COVID-19 » fundraising campaign of Institut Pasteur., Martel, Anne-Sophie, UFR Médecine [Santé] - Université Paris Cité (UFR Médecine UPCité), Centre National de Référence des virus des infections respiratoires (dont la grippe) - National Reference Center Virus Influenzae [Paris] (CNR - laboratoire coordonnateur), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Université de Paris - UFR Médecine Paris Centre [Santé] (UP Médecine Paris Centre), Université de Paris (UP), Institut Pasteur [Paris], Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and École nationale vétérinaire d'Alfort (ENVA)

Subjects
0301 basic medicine, Male, Epidemiology, Cross-sectional study, viruses, [SDV]Life Sciences [q-bio], Disease, medicine.disease_cause, Antibodies, Viral, Serology, Coronavirus OC43, Human, 0302 clinical medicine, 030212 general & internal medicine, Child, skin and connective tissue diseases, Coronavirus, biology, virus diseases, OC43, Systemic Inflammatory Response Syndrome, 3. Good health, [SDV] Life Sciences [q-bio], Child, Preschool, Spike Glycoprotein, Coronavirus, Female, France, Seasons, Antibody, medicine.symptom, HKU1, Paris, Adolescent, Asymptomatic, 03 medical and health sciences, Immunity, Virology, medicine, Humans, Serologic Tests, 229E, business.industry, SARS-CoV-2, Research, Public Health, Environmental and Occupational Health, Infant, Newborn, Infant, COVID-19, medicine.disease, Systemic inflammatory response syndrome, 030104 developmental biology, Cross-Sectional Studies, NL63, biology.protein, business
Abstract

Background Children have a low rate of COVID-19 and secondary severe multisystem inflammatory syndrome (MIS) but present a high prevalence of symptomatic seasonal coronavirus infections. Aim We tested if prior infections by seasonal coronaviruses (HCoV) NL63, HKU1, 229E or OC43 as assessed by serology, provide cross-protective immunity against SARS-CoV-2 infection. Methods We set a cross-sectional observational multicentric study in pauci- or asymptomatic children hospitalised in Paris during the first wave for reasons other than COVID (hospitalised children (HOS), n = 739) plus children presenting with MIS (n = 36). SARS-CoV-2 antibodies directed against the nucleoprotein (N) and S1 and S2 domains of the spike (S) proteins were monitored by an in-house luciferase immunoprecipitation system assay. We randomly selected 69 SARS-CoV-2-seropositive patients (including 15 with MIS) and 115 matched SARS-CoV-2-seronegative patients (controls (CTL)). We measured antibodies against SARS-CoV-2 and HCoV as evidence for prior corresponding infections and assessed if SARS-CoV-2 prevalence of infection and levels of antibody responses were shaped by prior seasonal coronavirus infections. Results Prevalence of HCoV infections were similar in HOS, MIS and CTL groups. Antibody levels against HCoV were not significantly different in the three groups and were not related to the level of SARS-CoV-2 antibodies in the HOS and MIS groups. SARS-CoV-2 antibody profiles were different between HOS and MIS children. Conclusion Prior infection by seasonal coronaviruses, as assessed by serology, does not interfere with SARS-CoV-2 infection and related MIS in children.

Published
2021
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2. Different Clinical Presentations and Outcomes of Disseminated Varicella in Children With Primary and Acquired Immunodeficiencies

Author

Paul Bastard, Aurélien Galerne, Alain Lefevre-Utile, Coralie Briand, André Baruchel, Philippe Durand, Judith Landman-Parker, Elodie Gouache, Nathalie Boddaert, Despina Moshous, Joel Gaudelus, Robert Cohen, Georges Deschenes, Alain Fischer, Stéphane Blanche, Loïc de Pontual, Bénédicte Neven, Human genetics of infectious diseases : Mendelian predisposition (Equipe Inserm U1163), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Groupe de Pathologie Infectieuse Pédiatrique [Paris] (GPIP), Société Française de Pédiatrie (SFP), Hôpital Jean Verdier [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Hôpital Louis Mourier - AP-HP [Colombes], Hôpital Robert Debré, Institut de Chimie des Substances Naturelles (ICSN), Institut de Chimie du CNRS (INC)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Nutrition, croissance et cancer (U 1069) (N2C), Université de Tours-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), CHU Necker - Enfants Malades [AP-HP], Centre Hospitalier Intercommunal de Créteil (CHIC), Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Gestionnaire, HAL Sorbonne Université 5, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)

Subjects
Male, 0301 basic medicine, lcsh:Immunologic diseases. Allergy, Pediatrics, medicine.medical_specialty, [SDV.IMM] Life Sciences [q-bio]/Immunology, Adolescent, medicine.medical_treatment, Fulminant, Immunology, Disease, Antiviral Agents, 03 medical and health sciences, Fatal Outcome, 0302 clinical medicine, varicella, medicine, Humans, Immunology and Allergy, Child, innate immunity, Immunodeficiency, Original Research, Lung, Chickenpox, business.industry, Immunologic Deficiency Syndromes, Infant, Immunosuppression, primary immumunodeficiencies, medicine.disease, Rash, 3. Good health, 030104 developmental biology, medicine.anatomical_structure, Child, Preschool, Varicella Zoster Virus Infection, disseminated varicella, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, medicine.symptom, business, lcsh:RC581-607, Nephrotic syndrome, 030215 immunology, steroids
Abstract

International audience; Primary infection with varicella-zoster virus (VZV) causes chickenpox, a benign and self-limited disease in healthy children. In patients with primary or acquired immunodeficiencies, primary infection can be life-threatening, due to rapid dissemination of the virus to various organs [lung, gastrointestinal tract, liver, eye, central nervous system (CNS)]. We retrospectively described and compared the clinical presentations and outcomes of disseminated varicella infection (DV) in patients with acquired (AID) (n= 7) and primary (PID) (n= 12) immunodeficiencies. Patients with AID were on immunosuppression (mostly steroids) for nephrotic syndrome, solid organ transplantation or the treatment of hemopathies, whereas those with PID had combined immunodeficiency (CID) or severe CID (SCID). The course of the disease was severe and fulminant in patients with AID, with multiple organ failure, no rash or a delayed rash, whereas patients with CID and SICD presented typical signs of chickenpox, including a rash, with dissemination to other organs, including the lungs and CNS. In the PID group, antiviral treatment was prolonged until immune reconstitution after bone marrow transplantation, which was performed in 10/12 patients. Four patients died, and three experienced neurological sequelae. SCID patients had the worst outcome. Our findings highlight substantial differences in the clinical presentation and course of DV between children with AID and PID, suggesting differences in pathophysiology. Prevention, early diagnosis and treatment are required to improve outcome.

Published
2020
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3. The interplay of CDK4 and CDK6 in melanoma

Author

Nikolaus Schicher, Florian Bellutti, Coralie Briand, Markus Zojer, Karoline Kollmann, Stefan Blunder, and Christoph Hoeller

Subjects
0301 basic medicine, CDK4, CDK6, Angiogenesis, Xenotransplantation, medicine.medical_treatment, Biology, angiogenesis, 03 medical and health sciences, 0302 clinical medicine, melanoma, medicine, Transcriptional regulation, neoplasms, Gene knockdown, Cell growth, Melanoma, Cell cycle, PD0332991, medicine.disease, 3. Good health, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Cyclin-dependent kinase 6, Priority Research Paper
Abstract

The cyclin-dependent kinases CDK4 and CDK6 promote progression through the cell cycle, where their functions are considered to be redundant. Recent studies have identified an additional role for CDK6 in the transcriptional regulation of cancer-relevant genes such as VEGF-A and EGR1 in hematopoietic malignancies. We show that the CDK4/6 inhibitor PD0332991 causes a significant decrease in tumor growth in a xenotransplantation mouse model of human melanoma. shRNA knockdown of either CDK4 or CDK6 significantly reduces cell proliferation and impedes their migratory capacity in vitro, which translates into a strong inhibition of tumor growth in xenotransplantation experiments. CDK4/6 inhibition results not only in the pronounced reduction of cell proliferation but also in an impaired tumor angiogenesis. CDK6 knockdown in melanoma cell lines impairs VEGF-A expression and reduces the potential stimulation of endothelial cell growth. The knockdown of CDK4 ends in similar results. The effect is caused by changes of CDK6 localization, less CDK6 is detected on the VEGF-A promoter. Bioinformatic analysis of human melanoma patient data verifies the key role of CDK6 in tumor angiogenesis in melanoma. The results highlight the importance of the delicate balance between CDK4 and CDK6 in regulating the cell cycle and transcription.

Published
2019
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4. Efficacy of JAK1/2 inhibition in the treatment of chilblain lupus due to TREX1 deficiency

Author

Marie-Louise Frémond, Aurélia Carbasse, Bénédicte Neven, Coralie Briand, Yanick J. Crow, Lucienne Chatenoud, Darragh Duffy, Vincent Bondet, Gillian I. Rice, Didier Bessis, Stéphane Blanche, CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service d'immuno-hématologie pédiatrique [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Necker - Enfants Malades [AP-HP], Imagine - Institut des maladies génétiques (IMAGINE - U1163), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), Université Sorbonne Paris Cité (USPC), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), University of Manchester [Manchester], Immunobiologie des Cellules dendritiques, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University of Edinburgh, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Necker - Enfants Malades [AP-HP], Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), ANR-16-CE17-0005,GENMSMD,Dissection génétique de la Susceptibilité Mendélienne aux infections mycobactériennes chez l'homme(2016), and ANR-16-CE17-0010,IFNX,Investigation des interferonopathies type I humaine(2016)

Subjects
0301 basic medicine, Ruxolitinib, Immunology, Encephalopathy, Inflammation, General Biochemistry, Genetics and Molecular Biology, rehabilitation, 03 medical and health sciences, 0302 clinical medicine, Rheumatology, Downregulation and upregulation, Interferon, medicine, Immunology and Allergy, 030203 arthritis & rheumatology, Lupus erythematosus, Janus kinase 1, treatment, business.industry, medicine.disease, 3. Good health, 030104 developmental biology, Tyrosine kinase 2, inflammation, [SDV.IMM]Life Sciences [q-bio]/Immunology, medicine.symptom, business, medicine.drug
Abstract

The type I interferonopathies, Mendelian disorders characterised by constitutive upregulation of the type I interferon (IFN) pathway, are associated with a spectrum of phenotypes particularly involving the brain and the skin.1 Mutations in the 3′−5′ DNA exonuclease TREX1 were the first described cause of the severe encephalopathy Aicardi-Goutieres syndrome (AGS),2 of which acral vasculitic lesions are a well-recognised feature. Familial chilblain lupus (FCL) is the name given where such lesions occur in the absence of neurological disease.3 TREX1 dysfunction, due to biallelic loss of function or dominant negative heterozygous mutations, is postulated to lead to aberrant immune recognition of self-nucleic acids inducing the production of type I IFNs. These potent cytokines drive the expression of IFN-stimulated genes (ISGs) through the engagement of a common receptor and the subsequent activation of Janus kinase 1 (JAK1) and tyrosine kinase 2. We describe, to our knowledge for the first time, the efficacy of the JAK1/2 inhibitor ruxolitinib in a patient with TREX1-related skin disease. Parental consent was obtained for the use of ruxolitinib on a compassionate basis. The patient carried a previously recorded dominant negative heterozygous mutation in TREX1 (c.52G>A, …

Published
2018
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5. Successful haematopoietic stem cell transplantation in a case of pulmonary alveolar proteinosis due to GM-CSF receptor deficiency

Author

Cécile Pochon, Christophe Delacourt, Bénédicte Neven, Alessandra Magnani, Alice Hadchouel, Despina Moshous, Coralie Briand, Laureline Berteloot, Alain Fischer, Stéphane Blanche, Cyril Schweitzer, Julie Bruneau, Jacques de Blic, Guilhem Cros, Marie-Louise Frémond, Marina Cavazzana, Cécile Bonnet, and Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)

Subjects
0301 basic medicine, Pulmonary and Respiratory Medicine, Pathology, medicine.medical_specialty, medicine.medical_treatment, Hematopoietic stem cell transplantation, Pulmonary Alveolar Proteinosis, 03 medical and health sciences, 0302 clinical medicine, Oxygen therapy, medicine, Humans, X chromosome, ComputingMilieux_MISCELLANEOUS, [SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/Pediatrics, medicine.diagnostic_test, business.industry, Hematopoietic Stem Cell Transplantation, Infant, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Hypoxia (medical), medicine.disease, 3. Good health, Transplantation, Haematopoiesis, 030104 developmental biology, Bronchoalveolar lavage, 030228 respiratory system, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, Female, medicine.symptom, Pulmonary alveolar proteinosis, business
Abstract

Cyril Schweitzer (CS) : A 1.5-year-old girl was referred to the Paediatric Pneumology Department of the University Hospital of Nancy, France, for progressive tachypnoea and hypoxia. She suffered from intrauterine growth retardation, and was born prematurely at 31 weeks’ gestation; birth weight: 1.160 kg (≤2 SD); birth length: 37 cm (≤2 SD). The patient presented with acute respiratory distress syndrome at birth, requiring treatment with a dose of surfactant, 9 days of mechanical ventilation and 8 weeks of oxygen therapy. On arrival to our centre, she was dyspnoeic on exertion and oxygen saturations were between 91% and 94%. Further investigations included a high-resolution CT scan and a bronchoalveolar lavage (BAL). Laureline Berteloot (LB) and Julie Bruneau (JB) : CT imaging of the chest revealed a ‘crazy paving’ pattern whereas analysis of BAL fluid failed to identify any underlying disease. CS : Hypoxia transiently improved after initiation of inhaled corticosteroids and antireflux therapy but relapsed after a few months, so that a second BAL was performed. JB : The second BAL fluid revealed the presence of extracellular lipid and protein deposits and foamy alveolar macrophages. CS and Cecile Bonnet (CeB) : These abnormalities led to a diagnosis of pulmonary alveolar proteinosis (PAP) at the age of 2.6 years, which was confirmed by genetic testing; complex chromosome abnormalities were detected, with (1) deletion of CSF2RA and CRLF2 on the X chromosome inherited from the mother, and (2) a de novo rearrangement of the paternal X chromosome, resulting in loss of both CSF2RA alleles.1 CS, Christophe Delacourt (CD) and Jacques De Blic (JDB) : Recessive mutations in the α or β subunits of the granulocyte macrophage colony-stimulating factor receptor (GM-CSF-R, encoded respectively by CSF2RA and CSF2RB ) cause two subtypes of hereditary PAP.2 Impairment of GM-CSF-dependent surfactant clearance by alveolar macrophages leads to the progressive accumulation of surfactant in the alveolar space …

Published
2018
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