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Updated: Jun 13, 2026
08:32
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Herpesvirus-encoded GPCRs rewire cellular signaling
Erik Slinger1, Ellen Langemeijer, Marco Siderius
1Leiden/Amsterdam Center for Drug Research (LACDR), Division of Medicinal Chemistry, Faculty of Sciences, Vrije Universiteit, De Boelelaan 1083, 1081 HV Amsterdam, The Netherlands.
Molecular and Cellular Endocrinology
|April 20, 2010
Summary
Viral G-protein-coupled receptors (vGPCRs) hijack host genes, influencing viral infections and pathologies. Understanding how these viral receptors rewire cellular networks is key to treating virus-associated diseases.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Viral G-protein-coupled receptors (vGPCRs) are viral homologs of host chemokine receptors.
- Encoded by Herpes- and Capripoxviridae, vGPCRs are believed to originate from the host genome.
- vGPCRs play critical roles in viral replication, pathogenesis, and immune evasion.
Purpose of the Study:
- To investigate the role of vGPCRs in viral infections and associated diseases.
- To understand how vGPCRs modulate host cellular signaling pathways.
- To identify vGPCRs as potential therapeutic targets for virus-associated pathologies.
Main Methods:
- Comparative genomics to identify vGPCRs.
- Molecular biology techniques to study vGPCR function.
- Cellular signaling assays to analyze pathway activation.
Main Results:
- vGPCRs contribute to immune evasion by interfering with host surveillance.
- Certain vGPCRs, like those from KSHV, EBV, and HCMV, are linked to persistent infections and cancer.
- vGPCRs activate signaling pathways promoting cell proliferation and inflammation, and induce growth factor secretion.
Conclusions:
- vGPCRs significantly alter host cellular signaling networks.
- Delineating vGPCR-modulated signaling is essential for developing treatments for viral diseases.
- Targeting vGPCRs offers a promising strategy for managing virus-associated pathologies.
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