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Friday, July 4, 2014

Helicobacter Pylori and Homo Erectus


I am posting once again on the Helicobacter Pylori bacteria, because I came across a paper while researching on Homo erectus in Southern Asia for my recent series on Y chromosome C haplogroup.


My previous post in case you are interested is this one: Ulcer causing bacteria and Neanderthals in America.


H. Pylori and Homo erectus


H. pylori are a type of bacteria that is found in the stomachs of roughly 66% of mankind. Its name "helicobacter", comes from its shape ("Helico" means "spiral").


People usually pick it up during childhood and in general it lives in its host unnoticed but, in certain people it causes disease (ulcers, inflamation or gastritis and in some cases, cancer).


It spreads from one person's mouth to another, so it quickly passes from parents to children and is exchanged between siblings as well as between couples. Another form of transmission is through contact with feces due to lack of hygene (a person who does not wash his or her hands after using the toilet). It can also be picked up from contaminated water or food.


Risk is higher in developing countries, but in the past, overcrowded conditions, lack of access to clean water and poor hygene allowed for an ample transmission within geographic localities and the people inhabiting them.


For this reason, it spreads rapidly within a population and is also affected by natural selection however this does not completely erase its origin.


Comment on Natural Selection.
The original American variety of H. pylori (known as hspAmerind) was specialised in infecting Native American hosts, when Europeans arrived (1492), the dramatic drop in native population due to war and disease plus the increase of Europeans and their "mestizo" mixed Amerind-European offspring allowed the more generalised European H. pylori (hspEurope) to outcompete it and greatly replace it.


This familial transmission keeps the different varieties of H. pylori within certain social groups (obviously those who live, share food, toilets, water and have sex together). This allows it to be used to study the prehistoric migrations of human beings with H. pylori in their stomachs.


Our most distant ancestors carried it in their gut, and as H. habilis evolved into our archaic ancestors (Neanderthals, H. erectus, H. heidelbergensis, etc.), H. pylori was in their stomachs, evolving too and passing along the evolving line of hominins till it reached us and (as orthodoxy states), left Africa some 60 kya in the wave of H. sapiens that would people the world and replace any other hominins out there. These human migrants settled in different regions and their H. pylori also evolved separately from those in the bellies of other humans in other places.


This is attested by the fact that there are different varieties of the bacteria specific to different geographic locations: [1]

  • hpNEAfrica, from Northeast Africa.
  • hpAfrica1, found in Western and Southern Africa.
  • hpAfrica2, only found in South Africa.
  • hpEurope, found in Europe, Western Asia, the Middle East, India and Iran.
  • hpAsia2, from Northern India, Bangladesh, Thailand and Malaysia.
  • hpEastAsia, found in Japan, Korea, Taiwanese Chinese, China and Vietnam.
  • hpSahul, carried by natives in Papua New Guinea and the Australian Aboriginals.
  • hspMaori, found among Melanesians, Taiwanese Aboriginals and Polynesians.
  • hspAmerind, carried by Native Americans.

This is interesting and points out closed groups moving with their own bacterial strains into the territories they peopled. But it also shows links between them that are not so clearly revealed by the human genome studies (mtDNA or Y chromosme sequencing). Below is Figure 2., from [1], the interesting part is not the map, but the trees:


Helicobacter pylori in Asia map
H. pylori Asian strain, in Asia and tree. From [1]

The captions from the original text are: "(A) Map of sampling locations of hspEAsia haplotypes in Southeast Asia... (B) Neighbor-joining tree from pair-wise FST values of hpEastAsia haplotypes rooted with haplotypes of the population hpSahul. (C) Neighbor-joining tree of pair-wise FST values of the subpopulation hspEAsia. doi:10.1371/journal.pone.0022058.g002" [1].


Look at B and C, the hspAmerind is completely separate from all the Asian and Melanesian - Polynesian branches. Very distinct indeed. They split off long ago, close to the split with hspSahul.


Looking at it from the perspective of my last post NRY haplogroup C, Eurasia and Homo erectus It is clear that hspMarori does not reflect the ancient C2 Y chromosome hapoltype of NG, instead it reflects the later arrivals from Taiwan. hspSahul on the other hand does reflect the archaic people that occupied Sahul with the C4 and C2 haplotypes. HspEAsia reflects C1 (Japan), C3 and C*. So clearly hspAmerind is the ancient C haplotypes found in America.


What about the Indian C5? and C-M130 marker, or the archaic European C6?


Let's look at the other figure from [1]:


HspEurope in Asia map
hspEurope in Asia, map and Tree. From [1]

European varieties split into two main branches North Europe (top) and France - Spain (bottom). The La Braña remains (7 ky old) with C6 haplotype were found in Spain.


The hspEurope is also found in Asia: in India and S.E Asia. This is what the paper (Breurec S., et al., 2011) [1] deals with in detail, trying to find out how did a specifically European variety of H. pylori reach the heart of South East Asia. The conclusions are remarkable:


Since it is found at high frequencies among Khmer (52%) and the variety was similar to the one found among Thais, but different to the French type, it is clear that it was not introduced into those populations due to Colonial contact with the French in Indochina (Vietnam, Laos, Cambodia), it is far older, and the paper suggests that "hpEurope bacteria in Southeast Asia might be a marker for an old human migration that predated the European colonial history." [1]


The link, as can be seen in the neighbor-joining tree (based on these pairwise FST values), shown above clusters the S.E. Asian and Indian varieties in a distinct group linked to the European types.


Recent introduction by Indians into S.E. Asia is also discarded because Malays, Thai and Khmer are closer to each other than to the Indians (from India or those that migrated to Malaysia).


Once again the paper concludes that this "suggest[s] a common origin of these strains and argu[e] against an exclusively recent acquisition of Malaysian hpEurope strains from Indian immigrants..." [1]. I fully agree, these are ancient strains that somehow were introduced into the region and prevailed despite the introduction of the hspEAsia.


The question is when did they reach Southeast Asia. The paper supports a two stage arrival: one to India and another onwards, into S.E. Asia: "an old introduction of hpEurope strains into the Indian subcontinent by Indo-Aryan migration (4000–10000 BP) as previously described. This was followed by subsequent eastward migrations of their descendants into Southeast Asia, carrying hpEurope strains in their stomach, probably within the last 3000 years." [1].


I disagree with both dates; they are too recent. Furthermore, allow me to quote another paper on H. pylori in the region (Tay et al., 2009): "there is no evidence that ancestral Malays migrated from India [or evidnece that] supports Malays sharing direct common ancestry with Indians." [2].


The paper adds: "Therefore for the Malay population, the ancestry of H. pylori does not reflect human ancestry as in other populations." [2]. I fully agree, it does not reflect the human ancestry of these people but their archaic ancestral Homo erectus ancestry.


Tay et al., are at a loss to explain the Indian - Malaysian link, and bogged down by the constraints of orthodoxy overlook the most parsimonious explanation. I will quote the paper (bold is mine):


"Another potential source of H. pylori for non-aboriginal Malays is the Orang Asli population, who originated from early human migration out of Africa.
The Orang Asli is likely to have taken the "Southern Route" into South East Asia to reach Malaysia by traveling along the Indian Ocean Coast line 50–65,000 years ago.
Therefore the Orang Asli H. pylori, if it exists, may share common ancestry with the Indian H. pylori, leading to the observed similarity of Malay isolates to Indian isolates.
"
So far so good, that is exactly the correct explanation, but then they dismiss it!.
"However given that other earlier H. pylori populations such as the Maori and American Indian populations can be readily identified, one would expect that the Orang Asli H. pylori population would be unique and identifiable after such a long period of separation, arguing against acquisition from Orang Asli population and in favour of acquisition from the Indian population." [2]


Actually the Orang Asli H. pylori and that of all S. E. Asians as well as the Indians, is the original archaic hspEurope in its "Asian Clade" as shown in the figure above.


Proof of the ancient origin of the Indian clade of hspEurope is found in S Manjulata Devi et al., (2007) [3], who were cited by [2] above, and who wrote: (bold mine)


"we suggest that H. pylori might have arrived in India probably at the same time when Indo-European language speaking people crossed into India (~4000–10,000 years before present). Alternatively, the unquestionable common origin of Indian strains with the European ones could be actually more ancient, following the upper Paleolithic spread of Homo sapiens in Eurasia, as suggested by mtDNA variability, and our data on H. pylori MLST do not rule out this possibility." [3]


This is where Breurec S et al., picked their date of 10 - 40 ky, but it is clear that S Manjulata Devi admits that an earlier date is possible, the actual OoA event into Asia.


The uniform dispersal within distinct geographic locations is in my opinion a clear indicator of an extremely ancient relationship between H. pylori and hominins, one that reflects, in my opinion, the most ancient dispersal of humans from Africa, the OoA event of H. erectus and their migrations.


The African diversity reflects perhaps even more ancient roots. But in Eurasia and the Americas the H. pylori lineages mirror the Y chromosome C haplogroup regions. As I conjectured in my previous post:


Current C hg. distribution reflects the migration of Homo erectus out of Africa 1.8 Mya. A band of a few hundreds of people walking into Asia with the CF haplogroup, splitting in the Persian Gulf by acquiring the M130 marker, and thus forming C haplogroup. They moved across South Asia keeping their C hg. identity during their long trek (note that since mutation rates are slower than accepted, no mutations arose during this period).


Finally reaching the Homeland from which it differentiated into its current haplogroups, in the North of S. E. Asia. From there they spread out. Some moved into NG, Australia mutating (slowly) into C2 and C4. Others went back into India and mutated to C5. The core in S.E. Asia evolved into C* while others went north forming C1 and C3.


A group did not take the Eastern route and went West into Europe forming C6 there. Maybe it will be sequenced someday from the bones at Sima de los Huesos...


Erectus entered America long ago, and the patchy C3* distribution in South America is what remains of a once widespread coverage of H. erectus in the New World...


So we see the correlation: hpEurope = C6, hpAsia2 = C5 - C* hpEastAsia = C3 - C1, hpSahul = C2, C4, hspMaori = C2 (Polynesia), hspAmerind = C3 (America).


Sources


[1] Breurec S, Guillard B, Hem S, Brisse S, Dieye FB, et al., (2011). Evolutionary History of Helicobacter pylori Sequences Reflect Past Human Migrations in Southeast Asia. PLoS ONE 6(7): e22058. doi:10.1371/journal.pone.0022058
[2] Tay CY, Mitchell H, Dong Q, Goh KL, Dawes IW, et al., (2009).Population structure of Helicobacter pylori among ethnic groups in Malaysia: recent acquisition of the bacterium by the Malay population. BMC Microbiol 9: 126. doi:10.1186/1471-2180-9-126
[3] S Manjulata Devi, et al., (2007). Ancestral European roots of Helicobacter pylori in India. BMC Genomics 2007, 8:184 doi:10.1186/1471-2164-8-184



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