Sarah Gerlo

Ghent University Hospital

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Jan Tavernier

Ghent University

Guy Haegeman

Ghent University

Sandra Van Lint

Ghent University Hospital

Anje Cauwels

Ghent University

Gilles Uzé

Centre National de la Recherche Scientifique

Ron Kooijman

Vrije Universiteit Brussel

Niko Kley

Forma Therapeutics (United States)

José Van der Heyden

VIB-UGent Center for Medical Biotechnology

Dominiek Catteeuw

Ghent University

Yann Bordat

Centre National de la Recherche Scientifique

Cooperative Institutions

Institute of Molecular Biology and Biophysics

254

Ghent University

169

Ghent University Hospital

129

Vlaams Instituut voor Biotechnologie

KU Leuven

VIB-UGent Center for Medical Biotechnology

VIB-UGent Center for Inflammation Research

Cancer Research Institute Ghent

Harvard University

Vrije Universiteit Brussel

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Organ-specific genome diversity of replication-competent SARS-CoV-2

Nature Communications (2021)

Jolien Van Cleemput Willem van Snippenberg Laurens Lambrechts Amélie Dendooven Valentino D’Onofrio

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is not always confined to the respiratory system, as it impacts people on a broad clinical spectrum from asymptomatic to severe systemic manifestations resulting in death. Further, accumulation of intra-host single nucleotide variants during prolonged SARS-CoV-2 infection may lead to emergence of variants of concern (VOCs). Still, information on virus infectivity and intra-host evolution across organs is sparse. We report a detailed virological analysis of thirteen postmortem coronavirus disease 2019 (COVID-19) cases that provides proof of viremia and presence of replication-competent SARS-CoV-2 in extrapulmonary organs of immunocompromised patients, including heart, kidney, liver, and spleen (NCT04366882). In parallel, we identify organ-specific SARS-CoV-2 genome diversity and mutations of concern N501Y, T1027I, and Y453F, while the patient had died long before reported emergence of VOCs. These mutations appear in multiple organs and replicate in Vero E6 cells, highlighting their infectivity. Finally, we show two stages of fatal disease evolution based on disease duration and viral loads in lungs and plasma. Our results provide insights about the pathogenesis and intra-host evolution of SARS-CoV-2 and show that COVID-19 treatment and hygiene measures need to be tailored to specific needs of immunocompromised patients, even when respiratory symptoms cease.

Viremia

Infectivity

Vero cell

Coronavirus

Pandemic

Pathogenesis

10.1038/s41467-021-26884-7

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Citations (64)

Correction: β-Agonists Selectively Modulate Proinflammatory Gene Expression in Skeletal Muscle Cells via Non-Canonical Nuclear Crosstalk Mechanisms

PLoS ONE (2023)

Krzysztof Kolmus Marleen Van Troys Karlien Van Wesemael Christophe Ampè Guy Haegeman

[This corrects the article DOI: 10.1371/journal.pone.0090649.].

Crosstalk

Proinflammatory cytokine

Non canonical

10.1371/journal.pone.0287938

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Citations (0)

Proinflammatory stimuli and β2-adrenoreceptor agonists synergistically induce IL-6 expression in myotubes

Krzysztof Kolmus Anneleen Spooren Karlien Van Wesemael Guy Haegeman Sarah Gerlo

Proinflammatory cytokine

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β2-Adrenergic receptors in immunity and inflammation: Stressing NF-κB

Brain Behavior and Immunity (2014)

Krzysztof Kolmus Jan Tavernier Sarah Gerlo

10.1016/j.bbi.2014.10.007

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Citations (106)

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Journal of Biological Chemistry (2014)

Jae Min Lee Umut Özcan Rachel Liberman Sarah Bond Mara G. Shainheit

On The CoverConfocal microscopy image of a ventricular myocyte from an adult rat heart, with nuclei stained with DAPI (blue) and cardiac myosin-binding protein C (green) and telethonin (red) immunolabeled with specific antibodies.Telethonin is localized to the Z-disc regions of cardiac sarcomeres, where its function may be regulated by phosphorylation of two Ser residues in the C-terminal region of the protein.For details see the article by Candasamy et al., pages

10.1016/s0021-9258(20)33659-0

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Figure S4 from Delivering Type I Interferon to Dendritic Cells Empowers Tumor Eradication and Immune Combination Treatments

Anje Cauwels Sandra Van Lint Franciane Paul Geneviève Garcin Stefaan De Koker

Combination treatments of B16 tumors with Clec9A-mAFN do not cause toxicity, in contrast to combinations with WT mIFN.

Interferon type I

10.1158/0008-5472.22418085.v1

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Ubiquitin D Regulates IRE1α/c-Jun N-terminal Kinase (JNK) Protein-dependent Apoptosis in Pancreatic Beta Cells

Journal of Biological Chemistry (2016)

Flora Brozzi Sarah Gerlo Fabio Arturo Grieco Matilda Juusola Alexander Balhuizen

Pro-inflammatory cytokines contribute to pancreatic beta cell apoptosis in type 1 diabetes at least in part by inducing endoplasmic reticulum (ER) stress and the consequent unfolded protein response (UPR). It remains to be determined what causes the transition from "physiological" to "apoptotic" UPR, but accumulating evidence indicates that signaling by the ER transmembrane protein IRE1α is critical for this transition. IRE1α activation is regulated by both intra-ER and cytosolic cues. We evaluated the role for the presently discovered cytokine-induced and IRE1α-interacting protein ubiquitin D (UBD) on the regulation of IRE1α and its downstream targets. UBD was identified by use of a MAPPIT (mammalian protein-protein interaction trap)-based IRE1α interactome screen followed by comparison against functional genomic analysis of human and rodent beta cells exposed to pro-inflammatory cytokines. Knockdown of UBD in human and rodent beta cells and detailed signal transduction studies indicated that UBD modulates cytokine-induced UPR/IRE1α activation and apoptosis. UBD expression is induced by the pro-inflammatory cytokines interleukin (IL)-1β and interferon (IFN)-γ in rat and human pancreatic beta cells, and it is also up-regulated in beta cells of inflamed islets from non-obese diabetic mice. UBD interacts with IRE1α in human and rodent beta cells, modulating IRE1α-dependent activation of JNK and cytokine-induced apoptosis. Our data suggest that UBD provides a negative feedback on cytokine-induced activation of the IRE1α/JNK pro-apoptotic pathway in cytokine-exposed beta cells.

c-jun

BETA (programming language)

10.1074/jbc.m115.704619

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Citations (45)

Figure S5 from Delivering Type I Interferon to Dendritic Cells Empowers Tumor Eradication and Immune Combination Treatments

Anje Cauwels Sandra Van Lint Franciane Paul Geneviève Garcin Stefaan De Koker

Combining checkpoint inhibition with Clec9A-mAFN does not cause toxicity.

10.1158/0008-5472.22418082.v1

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Figure S5 from Delivering Type I Interferon to Dendritic Cells Empowers Tumor Eradication and Immune Combination Treatments