ArticleMolecular systems biology2022
Nonproductive exposure of PBMCs to SARS-CoV-2 induces cell-intrinsic innate immune responses.
Article in Molecular systems biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Peripheral immune progression to long COVID is associated with mitochondrial gene transcription: A meta-analysis.Mitochondrion · 2025Pooled it
- Deleterious variants in the autophagy-related gene RB1CC1/FIP200 impair immunity to SARS-CoV-2.Nature communications · 2025Article
- Multiple Mechanisms of Action of SulfodyneAntioxidants (Basel, Switzerland) · 2024Article
- Metacell-based differential expression analysis identifies cell type specific temporal gene response programs in COVID-19 patient PBMCs.NPJ systems biology and applications · 2024Article
- Altered mitochondrial respiration in peripheral blood mononuclear cells of post-acute sequelae of SARS-CoV-2 infection.Mitochondrion · 2024Article
- Article
- Diacerein reduces inflammasome activation and SARS-CoV-2 virus replication: a proof-of-concept translational study.Frontiers in pharmacology · 2024Article
- Development of an In Vitro Model of SARS-CoV-Induced Acute Lung Injury for Studying New Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2022Article
- Monocyte-crosstalk drives interferon-mediated signaling following SARS-CoV-2 exposure.Molecular systems biology · 2022Article
- Nonproductive exposure of PBMCs to SARS-CoV-2 induces cell-intrinsic innate immune responses.Molecular systems biology · 2022Article
- Dysfunctional purinergic signaling correlates with disease severity in COVID-19 patients.Frontiers in immunology · 2022Article
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17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell-intrinsic responses mounted in PBMCs during mild and severe COVID-19 differ quantitatively and qualitatively. Whether they are triggered by signals emitted by productively infected cells of the respiratory tract or result from physical interaction with virus particles remains unclear. Here, we analyzed susceptibility and expression profiles of PBMCs from healthy donors upon ex vivo exposure to SARS-CoV and SARS-CoV-2. In line with the absence of detectable ACE2 receptor expression, human PBMCs were refractory to productive infection. RT-PCR experiments and single-cell RNA sequencing revealed JAK/STAT-dependent induction of interferon-stimulated genes (ISGs) but not proinflammatory cytokines. This SARS-CoV-2-specific response was most pronounced in monocytes. SARS-CoV-2-RNA-positive monocytes displayed a lower ISG signature as compared to bystander cells of the identical culture. This suggests a preferential invasion of cells with a low ISG baseline profile or delivery of a SARS-CoV-2-specific sensing antagonist upon efficient particle internalization. Together, nonproductive physical interaction of PBMCs with SARS-CoV-2- and, to a much lesser extent, SARS-CoV particles stimulate JAK/STAT-dependent, monocyte-accentuated innate immune responses that resemble those detected in vivo in patients with mild COVID-19.
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