Experts recently discovered that elephants sometimes secrete and shed the virus in their trunks, but there’s no proof it’s transmitted that way. “We think it’s likely transmitted in bodily fluids, like saliva—most herpesviruses are,” says Hayward. “That said, it’s very unlikely that it’s passed through placenta, and there’s no evidence for it in semen.” That’s good news for those who fear that elephant-breeding programs put calves at risk. And with evidence that EEHV is a wild-born rather than captive-born disease, calves in zoos are at no greater risk than wild ones.
Scientists think it’s likely that all African elephants carry—but don’t die from—at least three viruses that are similar to EEHV1, the type that frequently kills Asians. When Richman first published her paper, the zoo community feared that the cohabitation of Africans and Asians in zoos meant that Africans were passing the virus to Asians. But when Asian elephants that had never been exposed to Africans—including wild calves in Asia—began dying from EEHV1, experts had to search elsewhere for a cause.
Hayward looks to evolution for an answer. Scientists have compared the DNA of all the EEHV types to the DNA of other herpesviruses. They’ve found that the EEHVs formed a distinct branch in the herpes family tree about 100 million years ago. They branched into the different EEHV types about 35 million, 20 million, and 10 million years ago.
Says Hayward: “Asian and African elephants became separate species between 4 million and 7 million years ago,” he says, “so it looks like the viruses have been with elephants from the beginning.”
Hayward believes the viruses were relatively harmless until at least 10,000 years ago. Then, he suggests, African elephants may have come into contact with Asians and passed along the deadly form of the virus. In that time, Asians and the virus simply haven’t evolved enough to adapt to each other.
“It’s not good for a virus to kill its host; that’s not how it’s supposed to work,” Hayward says. “Somewhere along the line, there was an accident. Now we’re having to deal with how to fix it.”
How to fix it—that’s the question.
The obvious solution is to create a vaccine, but attempts to grow the virus in cultures—the first step in developing a vaccine—have been unsuccessful. There are ways to make vaccines without growing the virus, but those are usually less effective. Still, Richman says, they would be better than nothing.
Because only a few hundred elephants would get the vaccine, it’s not a profitable endeavor. Richman spent years pitching the idea to drug companies, but none would do it. More recently, a few academic institutions have expressed interest.
Other research efforts are getting at the problem from different sides. Last year, scientists at Baylor College of Medicine developed a test that can detect EEHV1 more quickly and in smaller quantities than the National Zoo’s method. It’s also better able to identify false positives and can pick up traces of the virus in healthy elephants that are secreting it in their trunks—something no other test has been able to do.
“It seems that the earlier an elephant begins treatment, the higher its chance of survival,” says Dr. Paul Ling, one of the lead researchers at Baylor. “Our test shortens the time it takes to get a diagnosis and can detect the virus even before symptoms are apparent.”
Baylor researchers are also developing methods to understand the genomic structure of EEHV—methods that could, Ling says, have future payoff for decoding new human viruses and how they work.
Tim Walsh hopes to bring Baylor’s test to Washington this year. He’s submitted a grant proposal to cover the cost: $20,000 to $30,000 for the machine plus supplies and upkeep.
In the meantime, the National Zoo is focusing on other EEHV research. Erin Latimer is testing the blood serum from healthy captive elephants and looking for antibodies to EEHV1. Her project will map which elephants have been infected with what virus and may provide clues to how elephants fight off disease. There’s talk of banking the antibody-rich serum and using it as treatment.
Latimer also plans to work with researchers overseas to better understand treatment options. “We don’t know why famciclovir seems to work in some cases but not in others,” she says. “Is it the drug that’s working, or is it the supportive care—fluids, supplements—that’s turned these elephants around?”
Another zoo initiative: coordinating with researchers to get a better handle on herpesviruses in wild elephants. A 2009 report by the International Elephant Foundation said that the virus had been found in wild elephants in India, Cambodia, and Thailand. At least eight Asian-elephant calves had died from the disease. Such findings lend credence to Hayward’s evolutionary theory, but they don’t prove it. “The answer will come from looking at which EEHV types are in wild African elephants and which are the naturally evolved, adapted types in Asians,” he says.
Two years ago, Latimer helped Dr. Arun Zachariah, a veterinarian in Kerala, India, set up the first EEHV field lab. He became interested in the research after performing necropsies on wild elephants that had died suddenly. Like the lab at the National Zoo, his is kept busy by veterinarians who send him samples to test. Last year, Latimer brought supplies to a zoo in South Africa in hopes of getting a lab going there, too.
“We need to learn about the virus and how it works in its natural hosts so that we can better take care of our zoo animals and protect the species as a whole,” says Latimer. “But with so many unanswered questions, making that happen is proving to be another story altogether.”