COVID-19 progression and convalescence in common variable immunodeficiency patients show dysregulated adaptive immune responses and persistent type I interferon and inflammasome activation

Javier Rodríguez-Ubreva (), Josep Calafell-Segura, Celia L. Calvillo, Baerbel Keller, Laura Ciudad, Louis-François Handfield, Carlos de la Calle-Fabregat, Gerard Godoy-Tena, Eduardo Andrés-León, Regina Hoo, Tarryn Porter, Elena Prigmore, Maike Hofmann, Annegrit Decker, Javier Martín, Roser Vento-Tormo (), Klaus Warnatz () and Esteban Ballestar ()
Additional contact information
Javier Rodríguez-Ubreva: 08916 Badalona
Josep Calafell-Segura: 08916 Badalona
Celia L. Calvillo: 08916 Badalona
Baerbel Keller: University of Freiburg
Laura Ciudad: 08916 Badalona
Louis-François Handfield: Wellcome Genome Campus
Carlos de la Calle-Fabregat: 08916 Badalona
Gerard Godoy-Tena: 08916 Badalona
Eduardo Andrés-León: Consejo Superior de Investigaciones Científicas (IPBLN-CSIC)
Regina Hoo: Wellcome Genome Campus
Tarryn Porter: Wellcome Genome Campus
Elena Prigmore: Wellcome Genome Campus
Maike Hofmann: University of Freiburg
Annegrit Decker: University of Freiburg
Javier Martín: Consejo Superior de Investigaciones Científicas (IPBLN-CSIC)
Roser Vento-Tormo: Wellcome Genome Campus
Klaus Warnatz: University of Freiburg
Esteban Ballestar: 08916 Badalona

Nature Communications, 2024, vol. 15, issue 1, 1-21

Abstract: Abstract Common variable immunodeficiency (CVID) is the most prevalent primary immunodeficiency, marked by hypogammaglobulinemia, poor antibody responses, and increased infection susceptibility. The COVID-19 pandemic provided a unique opportunity to study the effects of prolonged viral infections on the immune responses of CVID patients. Here we use single-cell RNA-seq and spectral flow cytometry of peripheral blood samples before, during, and after SARS-CoV-2 infection showing that COVID-19 CVID patients display a persistent type I interferon signature at convalescence across immune compartments. Alterations in adaptive immunity include sustained activation of naïve B cells, increased CD21low B cells, impaired Th1 polarization, CD4+ T central memory exhaustion, and increased CD8+ T cell cytotoxicity. NK cell differentiation is defective, although cytotoxicity remains intact. Monocytes show persistent activation of inflammasome-related genes. These findings suggest the involvement of intact humoral immunity in regulating these processes and might indicate the need for early intervention to manage viral infections in CVID patients.

Date: 2024
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DOI: 10.1038/s41467-024-54732-x

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