|HLA-A11: the legacy of H. erectus in ourselves
|Please read the updates below because some of the claims may not be sustainable (however others are plausible).
Prof. Peter Parham (Stanford University, USA) has found that some of the most common immunologic alleles among non-African modern humans have been adopted from other species of Homo living in Eurasia upon the migration out of Africa.
This would be a typical case of introgression, a process in which, by means of lesser admixture highly adaptive alleles from another population are adopted. The logic here is that Neanderthals and other Eurasian hominins would be much better adapted to Eurasian-specific diseases, while our species would initially be adapted to African-specific diseases instead.
According to New Scientist:
One allele, HLA-C*0702, is common in modern Europeans and Asians but never seen in Africans; Parham found it in the Neanderthal genome, suggesting it made its way into H. sapiens of non-African descent through interbreeding. HLA-A*11 had a similar story: it is mostly found in Asians and never in Africans, and Parham found it in the Denisovan genome, again suggesting its source was interbreeding outside of Africa.
Half of European HLA-A alleles come from other hominins, says Parham, and that figure rises to 72 per cent for people in China, and over 90 per cent for those in Papua New Guinea.
The dominance of Denisovan alleles in Eastern Eurasia is coincident with my theory of these Denisovan specimens being hybrids of H. erectus and Neanderthals and acting actually as a proxy for H. erectus, with whom some of our ancestors would have hybridized in SE Asia, where this hominin is known to have existed until very late dates compatible with our arrival to the region.
Besides HLA, only Melanesians show some clear (albeit very minor) Denisovan
admixture, but in the realm of antigens
, the legacy of H. erectus has been clearly stronger.
News found thanks to Neanderfollia[cat].
See also in this blog:
John Hawks, who has also been studying HLA, has objections
to the conclusion that these alleles come from Denisovans or Neanderthals. For what I could gather he has two objections:
- Age estimates, which are high risk slippery terrain.
- Insufficient resolution of the genetics of the archaic hominin genomes.
Important Update (Jun 18): the “Neanderthal” allele probably Sapiens, the “Denisovan” one may stand:
Hawks (same post, updated or did I miss it in first read?) directs us to a database of allele frequencies through the World, which would seem a most useful reference site. There we get clear evidence that the “Neanderthal” allele HLA*C:0702 probably migrated with our ancestors from Africa and needs no introgression explanation at all. The allele is frequent enough in many African populations peaking among the Baka Pygmies with 15%.
More complicated is the case of the allegedly Denisovan (Erectus) alleles HLA*A11. A look at the database is very clear: no native African population (south of the Sahara) has it at all except the creole ones of Cape Verde and Sao Tome (where it has without doubt recent European origin) and, crucially, a sample from Kampala, Uganda, where it reaches 4.3%.
This sample one is the only one that could suggest an African origin for this set of haplotypes. It could be argued however that as some genetic back-flow from Asia exists in the area, this case is explained by genetic back-flow. However the apportion is rather high, almost as high as Moroccan Berbers, Italians or Macedonians. Even the largest possible Asian source (Omanis: 11.4%) does not seem to be large enough to justify this island of HLA*A11 in Kampala.
Additionally the Nilotic Nandi of nearby Kenya are reported to have 0% of the controversial alleles. It is really hard to explain how this island of HLA*A11 arose in Kampala. But on the other hand, the fact that it is such an isolated finding is equally suspicious: if the allele (essentially HLA*A11:01) was so old in Africa, we should expect it to be found at least a very low frequencies in other populations.
Fine that malaria or other tropical diseases may have played a contrary selective role, as Hawks argues, but still the allele could, should, have survived in populations not affected by this disease. Also Uganda is not less Malaria-prone than Kenya (or most other nearby countries). So this explanation is not satisfactory.
A very localized founder effect of Asian origin (or a reporting error maybe) would seem to be at the origin of this anomaly. Also no African presence of variants 02, 03 or 04 has ever been reported.
Of course, we must always await for further data and research, but on the grounds of what we have now, I would say that:
- Claim 1: HLA*C0702 is a Neanderthal introgressed allele. Busted!
- Claim 2: HLA*A11 (several alleles) is a Denisovan (Erectus probably) introgressed allele. Plausible (but watch that Kampala island in Africa).
Update (Aug 26):
The reference paper is:
Laurent Abi-Rached et al., The Shaping of Modern Human Immune Systems by Multiregional Admixture with Archaic Humans. Science, 2011. Pay per view.
The supplementary material however is freely available.