Abstract
Human cytomegalovirus (HCMV) retinitis accounts for 70% of herpesvirus-infected ocular diseases. Recent advances in knowledge of innate immune responses to viral infections have elucidated a complex network of the interplay between the invading virus, the target cells, and the host immune responses. Ocular cytomegalovirus latency exacerbates the development of choroidal neovascularization. Viruses have various strategies to evade or delay the cytokine response, and buy time to replicate in the host. Some signaling proteins impact the virologic, immunologic, and pathological processes of herpesvirus infection with particular emphasis on retinitis caused by HCMV. The accumulated data suggest that signaling proteins can differentially affect the severity of viral diseases in a highly cell-type-specific manner, reflecting the diversity and complexity of herpesvirus infection and the ocular compartment. By summarizing the immunological characteristics and pathogenesis of HCMV ocular infection, it will provide important information on the development of antiviral therapy, immunotherapy, and antidrug resistance.