Cytomegaloviruses (CMVs) have the ability to persist lifelong within the infected host. This ability implies that these viruses are highly adapted to their hosts. Most importantly, they will have to employ strategies to remain hidden from the host's immune system. Virus genes predicted to be involved in these strategies include genes encoding homologs of cellular immune effector or regulatory proteins, such as chemokine (CK) receptor-like G protein-coupled receptors (GPCRs), CKs and MHC class I molecules. These genes may have been pirated by the virus during the long co-evolution of pathogen and host. In light of the crucial roles that GPCRs, CKs and MHC class I molecules play in the normal physiology of the host, it is to be expected that the CMV homologs of these proteins may have a profound impact on this physiology and, at the same time, serve vital functions in maintenance as well as replication of the virus within the infected host. As a consequence, these viral homologs can be envisaged as attractive targets for novel anti-viral strategies. The aim of this report is to present an overview of the current state of knowledge on the (putative) functions of the CMV homologs of GPCRs and CKs.