from Klaus Früh, Daniel Malouli, Kristie L. Oxford and Peter A. Barry writing in Cytomegaloviruses: From Molecular Pathogenesis to Intervention:
The last few years have witnessed significant expansion of the Non-Human-Primate (NHP) models of CMV persistence and pathogenesis. Progress in the utilization of the NHP CMV models has been highlighted by a better understanding of natural history, comparative genomic sequence analyses, and in vivo studies addressing mechanisms of tissue tropism, immune modulation, vaccine development, and optimization of the use of CMV as a vaccine vector for ectopic expression of heterologous antigens. The earliest observations of CMV infection in NHP during the first part of the twentieth century were remarkable for their prescient descriptions of CMV-host relationships based entirely on microscopic characterization of the protozoan-like (cytomegalic) cells that had been noted in congenitally infected human infants (Ribbert, 1904; Goodpasture and Talbot, 1921) and guinea pigs (Jackson, 1920). In particular, it was noted in the 1920's and 1930's that NHP CMV (1) is a ubiquitous infectious agent, (2) infects multiple cell types, (3) is characterized by low virulence, and (4) modifies host inflammatory responses. In addition, the first use of the term "latency" to describe the ability of CMV to reactivate may have been used for NHP CMV. In 1935, Cowdry and Scott recognized that treatment of CMV-infected monkeys with irradiated ergosterol stimulated reactivation of CMV in multiple tissues, and they noted that the treatment "may have activated or intensified a process already latent in the kidneys" (Cowdry and Scott, 1935). The recent progress in the NHP models follows these earliest insights into the hallmarks of CMV infections, and now enables the unique positioning of NHP models to provide a better understanding, treatment, and prevention of HCMV infection and disease in humans. This review summarizes the current status of our understanding of NHP CMVs with particular emphasis on viral gene function and viral disease models.
Further reading: Cytomegaloviruses: From Molecular Pathogenesis to Intervention