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Articles by Wolfram Brune
Cytomegalovirus inhibitors of programmed cell death restrict antigen cross-presentation in the priming of antiviral CD8 T cells
Loading metrics Open Access Peer-reviewed Research Article ? This is an uncorrected proof. Citation: Ebert S, Böhm V, Büttner JK, Brune W, Brinkmann MM, Holtappels R, et al. (2024) Cytomegalovirus inhibitors of programmed cell death restrict antigen cross-presentation in the priming of antiviral CD8 T cells. PLoS Pathog 20(8): e1012173.
No Time to Die: How Cytomegaloviruses Suppress Apoptosis, Necroptosis, and Pyroptosis
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Cytomegalovirus inhibitors of programmed cell death prevent a contribution of antigen cross-presentation to the priming of antiviral CD8 T cells
Abstract CD8 T cells are the predominant effector cells of adaptive immunity in preventing cytomegalovirus (CMV) multiple-organ disease caused by cytopathogenic tissue infection. The mechanism by which CMV-specific, naïve CD8 T cells become primed and clonally expand is of fundamental importance for our understanding of CMV immune control.
Human cytomegalovirus glycoprotein variants governing viral tropism and syncytium formation in epithelial cells and macrophages
Abstract Human cytomegalovirus (HCMV) displays a broad cell tropism, and the infection of biologically relevant cells such as epithelial, endothelial, and hematopoietic cells supports viral transmission, systemic spread, and pathogenesis in the human host. HCMV strains differ in their ability to infect and replicate in these cell types, but the genetic basis of these differences has remained incompletely understood.
A cytomegalovirus inflammasome inhibitor reduces proinflammatory cytokine release and pyroptosis - Nature Communications
Abstract In response to viral infection, cells can initiate programmed cell death (PCD), leading to a reduction in the release of viral progeny. Viruses have therefore evolved specific mechanisms to curb PCD. Cytomegaloviruses (CMVs) are sophisticated manipulators of cellular defenses and encode potent inhibitors of apoptosis and necroptosis. However, a CMV inhibitor of pyroptosis has not been clearly identified and characterized.
Viral dew: Phase separation and the formation of viral replication compartments
Citation: Bosse JB, Brune W (2023) Viral dew: Phase separation and the formation of viral replication compartments. PLoS Pathog 19(2): e1011145. https://doi.org/10.1371/journal.ppat.1011145 Editor: Felicia Goodrum, University of Arizona, UNITED STATES Published: February 16, 2023 Copyright: © 2023 Bosse, Brune.
Cross-regulation of viral kinases with cyclin A secures shutoff of host DNA synthesis
Abstract Herpesviruses encode conserved protein kinases (CHPKs) to stimulate phosphorylation-sensitive processes during infection. How CHPKs bind to cellular factors and how this impacts their regulatory functions is poorly understood. Here, we use quantitative proteomics to determine cellular interaction partners of human herpesvirus (HHV) CHPKs. We find that CHPKs can target key regulators of transcription and replication.
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