Cytomegaloviruses (CMV) are β-herpesviruses that establish persistent, latent infection in their hosts. Human CMV (HCMV) infection causes significant morbidity and mortality in immunosuppressed patients, including transplant recipients. Additionally, HCMV infection exacerbates the development of transplant vascular sclerosis (TVS) and accelerates chronic rejection (CR) of solid organ transplants. Current therapies to control HCMV do not sufficiently prevent this exacerbation of disease, warranting further research. Here, we examine interactions between the host-immune response and CMV-encoded proteins during pathogenesis and viral dissemination, using a rat CMV (RCMV) infection model of rat cardiac transplantation.