RT Journal Article
SR Electronic
T1 A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.02.23.432486
DO 10.1101/2021.02.23.432486
A1 Camille de Cevins
A1 Marine Luka
A1 Nikaïa Smith
A1 Sonia Meynier
A1 Aude Magérus
A1 Francesco Carbone
A1 Víctor García-Paredes
A1 Laura Barnabei
A1 Maxime Batignes
A1 Alexandre Boullé
A1 Marie-Claude Stolzenberg
A1 Brieuc P. Pérot
A1 Bruno Charbit
A1 Tinhinane Fali
A1 Vithura Pirabarakan
A1 Boris Sorin
A1 Quentin Riller
A1 Ghaith Abdessalem
A1 Maxime Beretta
A1 Ludivine Grzelak
A1 Pedro Goncalves
A1 James P. Di Santo
A1 Hugo Mouquet
A1 Olivier Schwartz
A1 Mohammed Zarhrate
A1 Mélanie Parisot
A1 Christine Bole-Feysot
A1 Cécile Masson
A1 Nicolas Cagnard
A1 Aurélien Corneau
A1 Camille Bruneau
A1 Shen-Ying Zhang
A1 Jean-Laurent Casanova
A1 Brigitte Bader Meunier
A1 Julien Haroche
A1 Isabelle Melki
A1 Mathie Lorrot
A1 Mehdi Oualha
A1 Florence Moulin
A1 Damien Bonnet
A1 Zahra Belhadjer
A1 Marianne Leruez
A1 Slimane Allali
A1 Christèle Gras Leguen
A1 Loïc de Pontual
A1 Pediatric-Biocovid Study Group
A1 Alain Fischer
A1 Darragh Duffy
A1 Fredéric Rieux- Laucat
A1 Julie Toubiana
A1 Mickaël M. Ménager
YR 2021
UL http://biorxiv.org/content/early/2021/02/23/2021.02.23.432486.abstract
AB SARS-CoV-2 infection in children is generally milder than in adults, yet a proportion of cases result in hyperinflammatory conditions often including myocarditis. To better understand these cases, we applied a multi-parametric approach to the study of blood cells of 56 children hospitalized with suspicion of SARS-CoV-2 infection. The most severe forms of MIS-C (multisystem inflammatory syndrome in children related to SARS-CoV-2), that resulted in myocarditis, were characterized by elevated levels of pro-angiogenesis cytokines and several chemokines. Single-cell transcriptomic analyses identified a unique monocyte/dendritic cell gene signature that correlated with the occurrence of severe myocarditis, characterized by sustained NF-κB activity, TNF-α signaling, associated with decreased gene expression of NF-κB inhibitors. We also found a weak response to type-I and type-II interferons, hyperinflammation and response to oxidative stress related to increased HIF-1α and VEGF signaling. These results provide potential for a better understanding of disease pathophysiology.Competing Interest StatementThe authors have declared no competing interest.