Introduction

In this chapter, we describe the biological, ger.omic and genetic diversity of the herpesviruses and then discuss the mechanisms that have been used to generate their different genetic complements. We consider how recent work has expanded our view of the possible origins of the family, and finish by sketching out the limitations that studies of present-day herpesviruses impose on our understanding of herpesvirus evolution. We have limited citations of the literature to appropriate reviews and particularly pertinent research papers.

Herpesviruses are complex viruses of higher eukaryotes which have large linear double-stranded DNA genomes and replicate in the nuclei of host cells (Matthews, 1982; Minson, 1989). They have a characteristic appearance in the electron microscope: an icosahedral capsid of 162 capsomeres embedded in an amorphous protein layer (the tegument) which is surrounded by a protein-containing lipid envelope. Agents of this type have been isolated from a wide range of vertebrates, including bony fish, amphibians, reptiles, birds, marsupials and placental mammals. It is possible that herpesviruses also infect invertebrates such as oysters (Farley et at., 1972), but this has yet to be confirmed. Known hosts in addition to humans are largely those subjected to husbandry, and the best studied are infected by several different herpesviruses. For example, humans are hosts to at least seven herpesviruses, and horses to at least five. The ubiquity of members of this large virus family, coupled with the very high degree of host specificity exhibited by individual members, indicates that the herpesviruses have a long history of evolution in close association with their hosts.