Human cytomegalovirus exploits STING signaling and counteracts IFN/ISG induction to facilitate infection of dendritic cells

Bibiana Costa, Jennifer Becker, Tobias Krammer, Felix Mulenge, Verónica Durán, Andreas Pavlou, Olivia Luise Gern, Xiaojing Chu, Yang Li, Luka Čičin-Šain, Britta Eiz-Vesper, Martin Messerle, Lars Dölken, Antoine-Emmanuel Saliba, Florian Erhard () and Ulrich Kalinke ()
Additional contact information
Bibiana Costa: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Jennifer Becker: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Tobias Krammer: Helmholtz-Centre for Infection Research (HZI)
Felix Mulenge: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Verónica Durán: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Andreas Pavlou: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Olivia Luise Gern: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Xiaojing Chu: Centre for Individualised Infection Medicine (CiiM) & TWINCORE, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Yang Li: Centre for Individualised Infection Medicine (CiiM) & TWINCORE, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School
Luka Čičin-Šain: Helmholtz Centre for Infection Research
Britta Eiz-Vesper: Hannover Medical School
Martin Messerle: Hannover Medical School
Lars Dölken: University of Würzburg
Antoine-Emmanuel Saliba: Helmholtz-Centre for Infection Research (HZI)
Florian Erhard: University of Würzburg
Ulrich Kalinke: a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Human cytomegalovirus (HCMV) is a widespread pathogen that in immunocompromised hosts can cause life-threatening disease. Studying HCMV-exposed monocyte-derived dendritic cells by single-cell RNA sequencing, we observe that most cells are entered by the virus, whereas less than 30% of them initiate viral gene expression. Increased viral gene expression is associated with activation of the stimulator of interferon genes (STING) that usually induces anti-viral interferon responses, and with the induction of several pro- (RHOB, HSP1A1, DNAJB1) and anti-viral (RNF213, TNFSF10, IFI16) genes. Upon progression of infection, interferon-beta but not interferon-lambda transcription is inhibited. Similarly, interferon-stimulated gene expression is initially induced and then shut off, thus further promoting productive infection. Monocyte-derived dendritic cells are composed of 3 subsets, with one being especially susceptible to HCMV. In conclusion, HCMV permissiveness of monocyte-derived dendritic cells depends on complex interactions between virus sensing, regulation of the interferon response, and viral gene expression.

Date: 2024
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DOI: 10.1038/s41467-024-45614-3

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