Implications from Current Studies
Gary Hayward, (JH and NEHL)
The major implications and interpretations from the following current genetic research findings on elephant herpesviruses are that:
- There are different sets of multiple distinct species and subtypes of EEHVs and EGHVs that naturally infect either Asian or African elephants, most of which are non-pathogenic and are harbored in a quiescent “latent” state, but reactivate periodically as localized lung or skin nodules, or in saliva and trunk wash secretions.
- Both of the pathogenic EEHV1A and EEHV1B subtypes that have caused most cases of the acute systemic hemorrhagic disease in European and North American zoos, also appear likely to be ubiquitous and latent in wild Asian elephant populations, as well as in most wild-born adult captive Asian elephants.
- Prior infection of an Asian elephant calf with either EEHV1A or EEHV1B (whether symptomatic or asymptomatic) evidently does not protect against subsequent infection with the other subtype, but it may elicit sufficient immune responses to protect against disease.
- However, infection with one strain of either the EEHV1A or EEHV1B subtype probably does provide immune protection against subsequent infection with another strain of that same subtype.
- Factors that influence whether primary infection of a naïve Asian elephant calf leads to systemic disease or is asymptomatic, may include the timing of the primary transmission event relative to which particular other species or subtypes of EEHV the calf has already been exposed to (or not), including EEHV4 and EEHV5, and the age and weaning status of the calf as it pertains to levels of maternal antibodies.
- Although they cannot be ruled out, there is no compelling reason at present to suspect that inherited host genetic resistance, nor specific “pathogenic strains” of EEHV1A play any significant roles here, beyond the fact that EEHV1A>EEHV1B are apparently far more pathogenic in Asian elephant calves than are any of the other EEHV types.
Clearly, it is not yet known just why about 20% of Asian elephant calves are susceptible to devastating hemorrhagic disease upon primary infections with EEHV1 especially, whereas African elephant calves and the other 80% of Asians do not seem to have problems coping with their EEHV infections. As implied above, the timing and order of infections by the other EEHV species and levels of immune response to them seem likely to be important factors, and the simplistic notion of preventing infections is not likely to be either feasible or desirable. Similarly, the extent to which this disease is occurring currently in wild Asian elephant populations, and whether or not it is a newly emerging or ancient impediment to the long-term breeding success and survival of this highly endangered flag-ship species need to be determined. Much more research is required to evaluate what intervention steps might be possible and appropriate.