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. 2015 Mar 9;6:40. doi: 10.3389/fphar.2015.00040

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Copyright © 2015 de Munnik, Smit, Leurs and Vischer.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Viral G protein-coupled receptors can modulate cellular signaling by means of different mechanisms. vGPCR are expressed at the cell surface of HHV-infected cells. For most vGPCRs, canonical mechanisms of host cell modulation has been studied in detail and shows that vGPCRs can signal through G proteins (1) in a constitutively active manner (2). Chemokine binding might modulate constitutive signaling (3). Less knowledge is available on non-canonical mechanisms that involve the interaction of vGPCRs with proteins from the endocytic machinery (e.g., β-arrestin) (4). In addition, vGPCR may modulate the function of human GPCRs (5) or RTKs (6).