Elephants are among the most intelligent non-humans, arguably on par with chimpanzees, but both African and Asian elephants — which are separate species — are endangered. In 1995, 16-month old Kumari, the first Asian elephant born at the National Zoo in Washington, DC, died of a then-mysterious illness. In 1999, Gary Hayward of Johns Hopkins University and collaborators published their results identifying a novel herpesvirus, EEHV1 (Elephant Endotheliotropic Herpes virus1) as the cause of Kumari’s sudden death. They now show that severe cases like this one are caused by viruses that normally infect the species, rather than by viruses that have jumped from African elephants, which was their original hypothesis. Hayward’s latest research appears ahead of print in the Journal of Virology.
At the time of Kumari’s death, anti-zoo activists seized on the situation to call for abandoning all efforts to breed Asian elephants in zoos, as they claimed that zoos were spreading the deadly herpesvirus, says Hayward. Contrary to that, in the current research, “We showed that whereas some identical herpesvirus strains infected both healthy and diseased animals concurrently at particular facilities, the majority were different strains, and there has not been a single proven case of the same strain occurring at any two different facilities,” says Hayward. “Therefore, the viruses have not spread between zoos, and the sources of the viruses were most likely wild-born elephant herdmates. In fact, we also found the same disease in several Asian range countries, including in orphans and wild calves, and showed that the EEHV1 strains in India displayed the same genetic diversity as those in Western zoos.”
In the study, the researchers performed extensive DNA fingerprinting of the genetic signatures of all the known EEHV cases, including those in zoos, as well as samples of EEHV virus that were obtained from wild Asian and African elephants, says Hayward. For this DNA fingerprinting the research team developed a specific analytical technique, because these viruses cannot be grown in cell culture. In the process, they identified seven different species of EEHVs and multiple different subtypes of each. All these different herpesvirus species and subtypes had their own host, either the African elephant or the Asian elephant, and were natural, endogenous and found everywhere. For instance, several of these viruses are occasionally shed in trunk washes and saliva of most healthy asymptomatic adult Asian elephants.
Close monitoring of Asian elephant calves in zoos has so far enabled life-saving treatment for at least nine infected Asian calves, says Hayward, suggesting that such monitoring may ultimately enable determining why some animals become susceptible to severe disease after their primary EEHV1 infections, while most do not. “About 20% of all Asian elephant calves are susceptible to haemorrhagic disease [caused by herpesvirus], whereas symptomatic disease is extremely rare in African elephant calves under the same zoo conditions,” says Hayward.
According to Philip Pellett, of Wayne State University School of Medicine, Detroit: “The information gained in the new EEHV paper will be important for developing diagnostic tools for these viruses, and for developing therapeutic approaches to diseases caused by EEHV.”
Elephant populations have been plummeting. African elephants declined roughly from 10 million to half a million during the 20th century, due largely to habitat destruction, and intense poaching has since further decimated their numbers. The African elephant (Loxodonta africana) is currently listed as Vulnerable by the IUCN Red List of Threatened Species™. While the Asian elephant (Elephas maximus) is listed as Endangered. The Asian species, once in the millions, now number less than 50,000. They are threatened mostly by habitat fragmentation. Poaching is not an issue since they lack tusks.
The full paper will appear in the December issue of the Journal of Virology.
(Source: American Society for Microbiology press release, 08.10.2014)