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Cytomegalovirus (CMV) is a widespread pathogen that infects a majority of the world’s population by early adulthood with approximately 50-85% of individuals over 40 being seropositive [1,2]. CMV can establish a life-long infection with its host by becoming latent during the lysogenic stage of the viral life cycle in which the virus becomes dormant and the shedding and production of infectious virions ceases [3]. However, the virus can later re-enter the lytic stage of the viral life cycle when presented with certain environmental cues, such as stress, thereby triggering the production of viral progeny and resulting in an acute infection of the host. Immunocompetent individuals generally display no symptoms of acute CMV infection, but CMV can cause morbidity and mortality in those with weakened or not fully developed immune systems [4]. The clinical manifestations of CMV infections in those with weakened immune systems, include spiking fever, malaise, leucopenia, encephalitis, pneu‐ monitis, hepatitis, uveitis, retinitis, gastrointestinal disease and graft rejection [5,6]. If primary infection or reactivation of CMV occurs during pregnancy in women, serious complications will arise for the fetus or developing embryo. CMV is the leading cause of viral birth defects, including microcephaly, mental retardation, spastic paralysis, hepatosplenomegaly, anemia, thrombocytopenia, deafness, and optic nerve atrophy that subsequently leads to blindness [5, 7]. CMV is also responsible for 8% of infectious mononucleosis cases [8].

Cytomegalovirus Tegument Proteins and the Development of Novel Antiviral Therapeutics