Molecular Mimicry by Cytomegaloviruses

Abstract

Cytomegaloviruses (CMVs) are well known for their high prevalence rate within host populations as well as their ability to induce lifelong infections. To maintain a persistent and stable relationship with their host, CMVs have evolved various molecular mechanisms to both control host cell metabolism and evade immune surveillance. Among the viral gene products that are likely to be involved in these processes are homologues of cellular G protein-coupled receptors, MHC class I molecules and chemokines. The viral genes encoding these homologues have probably been pirated by the viruses during a long pathogen/host coevolution. In this report, we will discuss the possible functions of these homologues in the pathogenesis of CMV infections.