Viral G Protein-Coupled Receptors: Attractive Targets for Herpesvirus-Associated Diseases

Timo W.M. De Groof, Elizabeth G. Elder, Marco Siderius, Raimond Heukers, John H. Sinclair, Martine J. Smit

Research output: Contribution to JournalReview articleAcademicpeer-review


Herpesviruses are ubiquitous pathogens that establish lifelong, latent infections in their host. Spontaneous reactivation of herpesviruses is often asymptomatic or clinically manageable in healthy individuals, but reactivation events in immunocompromised or immunosuppressed individuals can lead to severe morbidity and mortality. Moreover, herpesvirus infections have been associated with multiple proliferative cardiovascular and post-transplant diseases. Herpesviruses encode viral G protein-coupled receptors (vGPCRs) that alter the host cell by hijacking cellular pathways and play important roles in the viral life cycle and these different disease settings. In this review, we discuss the pharmacological and signaling properties of these vGPCRs, their role in the viral life cycle, and their contribution in different diseases. Because of their prominent role, vGPCRs have emerged as promising drug targets, and the potential of vGPCR-targeting therapeutics is being explored. Overall, these vGPCRs can be considered as attractive targets moving forward in the development of antiviral, cancer, and/or cardiovascular disease treatments. SIGNIFICANCE STATEMENT: In the last decade, herpesvirus-encoded G protein-coupled receptors (GPCRs) have emerged as interesting drug targets with the growing understanding of their critical role in the viral life cycle and in different disease settings. This review presents the pharmacological properties of these viral receptors, their role in the viral life cycle and different diseases, and the emergence of therapeutics targeting viral GPCRs.

Original languageEnglish
Pages (from-to)828-846
Number of pages19
JournalPharmacological reviews
Issue number2
Early online date10 Mar 2021
Publication statusPublished - 1 Apr 2021

Bibliographical note

Publisher Copyright:
Copyright © 2021 by The Author(s).

This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine


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