In the tragic battle against devil facial tumor disease (DFTD), scientists may have found the first “glimmer of hope” near Cradle Mountain in northwestern Tasmania. At least that is what Katherine Belov of the University of Sydney and colleagues are saying about this unique colony that has resisted the disease.
DFTD is a transmissible cancer spreading rapidly across Tasmania; it has caused a 90% decline in the total devil population. The northwestern colony, however, appears to be immune to DFTD through a unique genetic makeup that differs from the inflicted eastern devils. As Belov describes to the Associated Press, “We think these devils may be able to see the cancer cells as foreign and mount an immune response against them. We think more animals might survive in the wild than we initially thought.”
Tasmanian devils are known for having a very low diversity of immune genes, called major histocompatibility complex (MHC). MHC is found in most vertebrates and controls the ability of the species to resist infection: the more diverse the MHC levels, the stronger the immune system. Typically, in the case of Tasmanian devils, the low MHC diversity cannot serve as an adequate barrier for DFTD.
But, as the researchers describe in a recent edition of Proceedings of the Royal Society, the issue is more complex, and counterintuitive, than just the low MHC diversity levels. And the results have serious implications for current rescue efforts.
It turns out that most devils’ genetic makeup features parts of two separate genetic sequences, Group 1 and Group 2. Since DFTD has mutated to include parts of both Group 1 and Group 2 sequences, the disease enters undetected by the immune system. It is as if the immune system accepts the disease as part of the devil’s body since it appears to be the same familiar sequence of Group 1 and Group 2 genes.
The northwestern devils, however, only contain gene sequences from either Group 1 or from Group 2, giving them the advantage over the disease. In other words, if a devil with only Group 1’s sequence gets attacked by DFTD, its immune system will recognize the foreign Group 2 elements of the disease and resist it. While it seems counterintuitive at first, it is the limited gene structure in northwestern devils that appears to be preserving the colony.
Belov cautions, however, that this is not a cure, but a way to buy time and reevaluate current rescue efforts. As she says in the AP article:
I don’t think this means that we can sit back and go, ‘Everything is OK,’ because we’ve already seen that the tumor has started to evolve. But now we can say that we’ve got a glimmer of hope. There may be some animals that may survive this epidemic.
Current rescue efforts focus on interbreeding devil colonies in an attempt to increase MHC diversity, which makes complete sense on the surface. But the researchers strongly recommend in the study that rescue programs keep the colonies isolated so the devils can fight off the diseases using their own unique MHC genes. In actuality, by breeding the devils, rescuers could be introducing the remaining 20% of healthy northwestern devils to the genetic diversity they would need to contract DFTD. That is, mixing colonies would introduce the complex MHC makeup of the eastern devils to the simplified, and paradoxically more resistant, northwestern devils.
Siddle, H., Marzec, J., Cheng, Y., Jones, M., & Belov, K. (2010). MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer Proceedings of the Royal Society B: Biological Sciences DOI: 10.1098/rspb.2009.2362