vendredi 21 décembre 2007
Partial DNA sequence analysis from blood and necropsy tissue has been carried out and is in progress in both my and Laura Richman’s laboratories over the past decade. To follow up on the point that Nancy Hawkes made, there is not yet a single instance in which we can state for certain that the virus that caused disease in one Asian juvenile elephant came from another specific individual source animal. In fact, the viruses involved are nearly all different from one another, in some cases hugely so at the level of different virus species or sub-species (EEHV1A, EEHV1B, EEHV2, EEHV3A, and EEHV3B) where some or all of the genes differ at the level of 10 to 40 percent in the protein amino acid structure, or at a low level (about 0.1 to 0.3 percent nucleotide differences) as distinct non-epidemiologically related virus isolates or variants from within the EEHV1A group itself.
These viruses all belong to the genus _Proboscivirus_, which must have co-evolved with their mastodon/elephantid hosts ever since they diverged from other mammalian groups. We project that the common ancestors of EEHV1/2 diverged from the EEHV3s about 25 million years ago, and EEHV1 and EEHV2 from each other about 10 million years ago (note that the last common ancestors of Asian and African elephants and the extinct woolly mammoths only diverged between 4 and 7 million years ago).
Furthermore, to further amplify Jim Wellehan’s comments, we now know of 11 different species or sub-species of elephant herpesviruses, which fall into 2 very different groups, the probosciviruses or EEHVs, and the elephant gammaherpesviruses discovered by Jim Wellehan. All 11 are found within the United States captive elephant population and they are all certain to also occur amongst the various wild populations of _Elephas maximas_, _Loxodonta africana_, and _Loxodonta cyclotis_, although we know little about which elephant species or sub-species is the natural host of which specific virus species. Of the 6 known _Probosciviruses_, 5 have been associated with fatal endotheliolytic disease — 4 in Asian elephants and one in African elephants — whereas none of the 5 known elephant gammaherpesviruses have yet been associated with disease, but at least one of the latter can be detected in almost all individual healthy elephants tested, as well as in some mucosal lesions.
With regard to specifics of the situations cited at the Woodland Park, Dickerson Park, Rockland, and Houston zoos : First, the species of virus that killed Hansa (EEHV3A) has only been seen in one other case (EEHV3B), but those 2 viruses are themselves 8 percent different, whereas the 2 old cases at Rockland where Rex is housed were both EEHV1A.
Secondly, among the 5 cases associated with Dickerson Park, Haji’s virus was a novel EEHV1A/EEHV1B chimera, and although the other 4 were all EEHV1A, we already know that Nisha’s is different from Kala’s. Haji was the 1st Asian calf bred by artificial insemination and yet we have seen no other case like it amongst the other progeny of Onyx.
Amongst those born in Houston, Kiba’s virus was EEHV1B (caught after transfer to Berlin, and his daughter Kiri in Berlin had EEHV1A). Also, although the sequence of the Kiba EEHV1B virus TER gene is quoted correctly as being 97 percent identical to the EEHV1As, other genes such as the TK are 40 percent different between EEHV1A and EEHV1B. Amongst the other 4 cases born at Houston, we know at least that Singgah’s virus was different from those of the cases that occurred at Rockland and at Lincoln Park, which were also both different from each other.
Similarly, among 2 cases at Oklahoma of progeny from the same mother and father, the 2 viruses were EEHV3B and an EEHV1. The 3 cases that were progeny of Thai and Methai included at least 2 different viruses (EEHV1A and EEHV1B) and the 5 cases that were progeny of Onyx have included EEHV3B, EEHV1A, and an EEHV1B.
Finally, the rapid acute systemic course in cases of elephant endotheliolytic disease almost certainly represents a primary infection in an immunologically naive juvenile animal. Therefore, it should be very obvious from the genetic analyses that the sources of the viruses that have caused disease have rarely if ever been the parents themselves (and are very also unlikely to be contracted from AI), but rather instead from sporadic close contacts with either wild-born animals that have carried their own specific virus in a latent state since infancy (which is the natural situation for virtually all herpesviruses within the hosts that they have co-evolved with), or possibly in carrier Asian elephants who may have caught and survived infection with the African EEHV1A virus asymptomatically as infants.
— Gary S. Hayward, PhD Viral Oncology Program Johns Hopkins School of Medicine, Baltimore, Maryland USA