Transmission Of Tuberculosis Is Linked To Historical Patterns Of Human Migrations

Contact: Maria A. Smit
smit@cshl.edu
1-516-422-4013
Cold Spring Harbor Laboratory

Transmission of tuberculosis is linked to historical patterns of human migration

St. Petersburg, Russia – Genghis Khan and his troops may have unwittingly used more than just brute military force to conquer entire nations and to establish the infamous Mongolian empire. A report in the October issue of Genome Research suggests that Genghis Khan's invasions spanning the continent of Asia during the 13th century may have been a primary vehicle for the dissemination of one of the world's most deadly diseases: tuberculosis.

In this study, a team of scientists led by Dr. Igor Mokrousov from St. Petersburg's Pasteur Institute demonstrated that the evolutionary history of the causative agent of tuberculosis (TB) has been shaped by human migration patterns.

The researchers examined the genetic signatures of over 300 strains of Mycobacterium tuberculosis, rod-shaped bacteria that, when airborne, infect the pulmonary systems of vulnerable individuals and give rise to clinical TB. The World Health Organization (WHO) estimates that TB kills 5,000 people worldwide every day, or approximately 2 million people each year. The pathogen is rapidly spreading and evolving multi-drug resistant strains in susceptible regions such as Africa. Interestingly, a strong gender bias in TB infection is reported globally each year; a 70% excess of male TB cases is typical.

"M. tuberculosis also has a remarkable ability to persist in the human host as a latent, asymptomatic form," explains Mokrousov. "This is probably what permitted M. tuberculosis to co-exist with humans during pre-industrialized times, when the primary mode of transmission was within families or households where there was significant physical contact." Today, approximately one-third of the world's population are carriers of latent TB.

Mokrousov's team hypothesized that, given the strong gender bias of TB infectivity and the likely family-based mode of TB transmission during pre-industrialized times, M. tuberculosis dissemination has reflected the unidirectional inheritance of the paternally transmitted human Y chromosome. To test this hypothesis, the authors compared the genetic profiles of a common form of M. tuberculosis, called the Beijing genotype, with known patterns of prehistoric and recent human migrations, as well as with global patterns of Y-chromosome variation. Strikingly, they observed that over the past 60,000-100,000 years, the dispersal and evolution of M. tuberculosis appears to have precisely ebbed and flowed according to human migration patterns.

The authors describe how the Beijing genotype of M. tuberculosis originated in a specific human population called the K-M9 in central Asia approximately 30,000-40,000 years ago following a second "out of Africa" migration event. The bacteria and its human host then disseminated northeast into Siberia between 20,000-30,000 years ago and throughout eastern Asia between 4,000-10,000 years ago. More recently, the Beijing genotype of M. tuberculosis was introduced into northern Eurasia, perhaps by Genghis Khan himself during the 1200's, and into South Africa, possibly through sea trade contacts with Indonesia or China during the last 300 years.

"The population structure of M. tuberculosis appears to have been shaped by the demographic history of its human carrier," explains Mokrousov, "but this is the opposite of what William McNeill suggested in 1976 in his famous book Plagues and Peoples, where he so popularly described how the growth and spread of infectious diseases such as the Black Death have influenced human history."

Mokrousov feels that these observations have important implications for tracing the evolutionary history of microorganisms. "The timing of hallmark changes in bacterial genomes within the last 100,000 years may be inferred from comparison with relevant human migrations," he says.

Interesting article, I'll post it:

Mitochondrial footsteps of the Old World human colonization: A single origin, several dispersal hypothesis.

José M. Larruga, Ana M. González, Nicole Maca-Meyer, Carlos Flores and Vicente M. Cabrera

Vicente Cabrera (29 October 2004) Department of Genetics, University of La Laguna

The hypothesis that Homo s. sapiens originated in Africa and later colonized Eurasia replacing the descendents of H. erectus is now widely accepted.
However, the timing of the exit out of Africa and the routes taken remain controversial. Archaeological and genetic evidence (Cavalli-Sforza et al. 1994) support two dispersals from Africa.
A southern migration that coasting Asia reached Australia, and a northern migration that reached Western Asia through the Near East.
Studies based on complete mitochondrial DNA sequences indubitably demonstrated that only two macrolineages, M and N, comprise all the mitochondrial variation existing out of Africa (Ingman et al. 2000; Maca-Meyer et al. 2001; Herrnstadt et al. 2002).
Based on the phylogeographic distribution of these two lineages and their derivates, with N prevalent in Europe and western Asia and M more frequent in southern and eastern Asia, we proposed that M and N were the mitochondrial signals of the southern and northern routes respectively (Maca-Meyer et al. 2001).
Recently, Palanichamy et al.(2004) disregarded our interpretation as simplistic and, based on new mitochondrial genome data of macrohaplogroup N in India, supported the more parsimonious hypothesis of a single migration route out of Africa proposed by others (Forster et al. 2001), but with the addition of another lineage, R, to that migration. So a scenario with a single migration route out of Africa and three-founder mtDNA lineages was defined.
In a recent article(Tanaka et al. 2004) the weakness of both hypothesis to congruently incorporate new mitochondrial data, mainly from Australia and Papua New Guinea (Ingman and Gyllensten 2003), was discussed suggesting that a new work hypothesis should be formulated to accomodate this recent information. Of main concern was the presence, in high frequencies, of macrohaplogroup N basal lineages in aboriginal Australians contrasting with its paucity in India and its absence in PNG.
If, as we proposed, N marks the northern route, how to explain its absence in southeast Asia and PNG, its natural path to Australia? On the other hand, if N was carried along with M in all routes how to explain its paucity in India and its absence in southeast Asia? Not to mention the lack of basal M in western Eurasia. In accordance, we have now modified our previous hypothesis.
In this second version we continue proposing at least two successive migrations from Africa. Anthropological studies show that Palaeolithic humans most probably moved in small groups with close familiar ties. This endogamic structure induces loss of variation.
So we think improbable that two divergent lineages such as M and N, separated by nine independent point mutations, were simultaneously carried by only one of those small groups.
In relation to R, it is a macro-haplogroup that comprises all the N lineages characterized by the reversion of 16223 and the presence of the 12705 substitution. So, it is phylogenetically derived from the basal N.
Until now, no authochtonous derived N lineages have been detected in Africa. Therefore, we suppose that R arose out of Africa.
It might be argued that the coalescence ages of the three macro-haplogroups are similar but the errors of these dates are so large that simultaneous or successive departures from Africa fit in them as well.

Now we think that the first successful group of modern humans leaving Africa mainly carried basal N lineages. Their spread out of Africa was global.
Climatic conditions should not have been insurmountable for groups that chose North, whereas others moved eastwards. R could have appeared before this split, going with N in both routes or, most probably, arose in the northern branch.
With time offshots of this northern trunk colonized Europe westwards, India southwards and, going eastwards, reached Northeast and Southeast Asia including PNG where R lineages have been detected (Ingman and Gyllensten 2003).

Relatively short in time, the second out of Africa human wave carried mainly basal M lineages. The lack of primitive M lineages in Europe and Central Asia suggests that this second migration found climatic dificulties to spread northwards or was adapted to exploit mainly marine resources choosing therefore a coastal migration (Stringer, 2000).
The southern route of M most probably followed the track of their N precursors, displacing and nearly substituting them in India and hastened their trail to Australia in spite of the maritime barriers found in this exodus.
M could have reached Australia following N but, most probably continued eastwards colonizing Southeast Asia and PNG originating, from this area, a second migration to Australia.
The independent histories of the human Y chromosomes from Melanesia and Australia (Kayser et al. 2001) are more in accordance with this second alternative.

We understand that the data in support of our hypothesis are meager at best.
However, it explains the currently observed geographic patterns of mtDNA variation fairly well. Of course, recurring to genetic drift and lineage extinctions other stories may also fit the present mtDNA phylogeography.
In any case, it is indispensable that any hypothesis can be testable. Studies of mitochondrial variability in southern and northern areas of India for R lineages could help to define the gate of entrance of this macro-haplogroup in India.
RFLPs distinguishing M from N lineages could be performed on the most ancient remains of aboriginal Australians to confirm that really these first immigrants belonged to macrohaplogroup N.
The same type of study applied to sinodont and sundadont Chinese remains would give information of their mtDNA adscription.

Finally, as predictably new N and R lineages will be detected in future studies of Southeast Asia and Oceania, we would like to suggest that those N and R lineages already found in Australia and PNG be named according to the widely accepted nomenclature system of Richards et al. (1998).

The Neandertal Enigma
by James Shreeve
"Allan Wilson had always been described to me in superlatives, such as 'one of the real geniuses in science,' or 'the most arrogant guy I know...' [H]e apologized for putting me off so long and bluntly explained that the reason he had done so was that he did not trust me... 'The anthropological perspective on evolution is no longer valid; it has been overthrown. And yet the science writers who insist on talking to me come drenched in an anthropological perspective, and there is really no point in talking to them... It is paralytic. It prevents you from asking certain questions, and it forces you to ask others. The whole discipline invites you not to investigate.'

...A few months before my visit, Wilson had announced at the annual meeting of the American Association for the Advancement of Science... that the Neandertals were replaced because they could not speak... suggesting that a particular gene for language might have been carried in the mitochondria themselves. Since invading males would have been more likely to mate with resident females than the other way around, the offspring of sexual contact between the two groups would be 'linguistically deaf-mute,' like their Neandertal mothers. Thus disadvantaged, these 'village idiots' would face the same fate as the mothers: extinction. Only the language-endowed African lineage would continue. The language gene idea, and especially the unfortunate term 'village idiots,' elicited hoots of derision from the anti-Eve camp, and gave no joy to Wilson's colleagues." [pp 119-121]

I don't think we disagree, but I'm not sure if my brief reference explained the extent of this guy's claim. Here is the opening line of a Reuters article back in 2002 about some of this research:

The idea of race is not reflected in a person's genes, Brazilian researchers report confirming what scientists have long said -- that race has no meaning genetically.

I have never cared about skin color in my entire life. Judgments based on skin color make about as much sense to me as deciding not to love your daughter because she came back from the beach with a tan.

However when two people who have the same skin color have kids there is this interesting tendency for their child to have the same skin color. This amazing trend seems to follow with greater and lesser frequency to eye color, hair color, various facial features, and even freckles.

We can look at someone and say they look Irish or Chinese or Italian. If genetics are not responsible for these similarities in characteristics that we all notice and use to categorize our world, it is a truly remarkable set of coincidences that all these children of people who belong to these nonexistent races keep developing features and traits that we mistakenly associate with that fictitious thing called race. Are all those genetic diseases that certain racial groups are at high risk for just some big scam?

I don't care about someone's skin color, but that doesn't mean that I agree with some agenda pushing scientist who claims skin color doesn't exist.

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