PATHOGENESIS
Latency is a common feature of the pathogenesis of all herpesvirus infections, although the site of latent infection typically varies according to the biological properties of the viruses in the different Subfamilies (Table 23.1).
During latency the herpesvirus genome typically becomes circular and only a small subset of genes is expressed. In this state the virus is able to largely evade host immune responses and no clinical signs are present. The viral and cellular mechanisms that enable herpesviruses to establish and reactivate from latency are not well known, but reactivation is typically associated with periods of host immune suppression, stress or concurrent infection. Reactivated (and primary) herpesvirus infections can then cause clinical disease and can be spread to other animals (Pellett and Roizman 2013). Experimental reactivation of macropodid alphaherpesvirus infection in eastern grey kangaroos has been demonstrated following high-dose corticosteroid administration to induce immunosuppression. The site of latency for these viruses has been identified as the trigeminal ganglia (Guliani et al. 1999). This reactivation from latency during periods of immune suppression or stress is particularly relevant for managed populations of marsupials, where capture-associated stress, overcrowding and close contact with other animals may lead to reactivation of herpesvirus infections and transmission to other animals to cause outbreaks of disease.Herpesviruses and their hosts have co-evolved for over 200 million yr (McGeoch et al. 2000). Frequently, these viruses do not cause severe disease unless the balance between host and virus is disrupted as described above. Another important context in which herpesviruses can cause severe disease is when they spillover from a natural
Fig. 23.1. Vesicular and ulcerative cloacitis in a zoo-housed tammar wallaby (Notamacropus eugenii) typical of lesions seen with macropodid herpesvirus infection. Photo: Timothy Portas
host species, for which they are evolutionarily adapted, to a new host species. This is particularly relevant for alphaherpesviruses (which have a more variable host range) in managed populations of marsupials where species may be held in close proximity with other species that they are not usually in contact with. This has been implicated in severe outbreaks of herpesvirus disease observed in managed brush-tailed bettongs, rufous bettongs (Aepyprymnus rufescens) and grey dorcopsis wallabies (Dorcopsis luctuosa) that were housed in close contact with other species of macropods (Dickson et al. 1980; Callinan and Kefford 1981; Wilks et al. 1981).
3.