The discovery, in 1973, of the association between ankylosing spondylitis and the Human Leukocyte Antigen HLA B27 raised two still unanswered questions. The first, the holy grail of spondyloarthropathy research, is simply; how does the B27 gene confer risk of developing the disease, and the second, somewhat less funded question; why the hell does this nasty piece of DNA still exist. Why haven't the Mendelian garbage collectors tossed this unwelcome gene onto the trash heap of failed genetic experiments.
Recent events have rekindled my interest in the latter question. The H1N1 influenza virus is upon us again and for unknown reasons appears to attack native populations with disproportionate ferocity. In Canada, many native communities have suffered greatly once the virus touches down. There is a higher number of affected and a much higher rate of severe infection. In some respects, it reminds me of the arrival of Europeans to the continent and their tallships laden with viruses which proved lethal to untold numbers of the original inhabitants. While the numbers vary wildly, it is suggested that up to 80% of the aboriginal population succumbed to one of the many waves of infectious diseases from abroad. Given this massive assault, it's possible that a small genetic survival advantage may have had a huge impact. Could that advantage have been the HLA B27? I'm starting to wonder. The clues that lead me to this suggestion start with the inordinately high rate of B27 amongst North American native populations. While most of the Northern native populations have higher rates of B27, the rate can run as high as 50% in some populations, such as the Haida of the west coast of Canada. And it isn't because they are immune to the arthritogenic potential of the gene. 20% of the men carrying the gene showed evidence of sacroiliitis on x-ray. Spondyloarthropathy would likely have been a brutal disease among these not-so-long-ago hunter-gatherer peoples, so why is it so prevalent? Could it be that the B27 gene somehow protected these vulnerable populations from the many plagues that followed the arrival of Europeans? The survivors, though cursed with this unfortunate gene may then have passed it on to future generations.
Sure, but it's just one of many possibilities. After all, B27 may simply be linked to any other gene with survival qualities, like hunting skills or negotiating with ethically challenged governments. On the other hand, there is some evidence that resisting infections is part of the B27 advantage. Recent studies have shown that HLA B27 has a protective effect in both HIV and Hepatitis C infections. While nobody suspects that either of these viruses had anything to do with the massive casualties post Columbus, it makes me wonder whether any of the other diseases such as smallpox or influenza were also less fatal among B27 carriers. It is known that HLA B27 is involved in the immune response to Influenza A, but I don't know whether this confers any survival advantage. In fact, it would be a very good study question. It might even be a good study question for the scary virus flying around the planet today.
Who knows. Maybe we'll all be begging for a B27 allele before the end of this modern day pandemic.