Review Population Genetics in Sudan

Abstract

When M. H. Satti embarked on a reconnaissance mission to monitor the visceral leishmaniasis (VL)
outbreak in the Blue Nile district in mid 1940s, he immediately realized the gravity of the situation. The
epidemic inflicted heavy toll on a small tribe called Jum Jum and almost decimated the very presence of
their existence(1). More than sixty years later pertinent questions are still justifiable on why the disease
would heavily affect a certain population but not others like the Jum Jum and Nuer who bore the brunt
of the 1980s and 1990s outbreak,(2) why a deadly disease becomes endemic to certain territory? why
epidemics suddenly erupt in a specified location? and why certain households and individuals are more
prone to encounter certain ailments?
DuringSatti’stimepopulationgeneticswas a fairlynewscience then,pioneeredbyoutstandingscientistslike J
BHaldane - aBriton also notorious of being an ardentsocialist activist.Haldane not only pioneered population
genetics but demonstrated the first examples of human adaptation through haemoglobinopathiesthat are still
the favourite showcaseof populationgenetics eventoday.Weknownowthat,the fateof anallele since its birth
in the form of a novel mutation/polymorphism is decided by a number of factors that includes beside natural
selection, a well-established paradigm by the 1930, other factors like migration, and genetic drift. Drift was
proposedbythe JapanesemathematicianMutoKimura andLucaCavalliSforza anItalianAmericangeneticist.
A similar situation faced A. M. Elhassan and his colleagues when they first set foot on the Rahad region
during early 1990s.(2) Elhassan was abhorred by the amount of suffering and misery caused by the disease.
The incidence was higher among certain ethnic groups, an observation also seen among game wardens in
the adjacent Dinder National Park.(3) The fact that the most vulnerable groups were mainly of Nilo-Saharan
speaking background from southern and northern Sudan, was irreconcilable with published evidence that
VL caused by Leishmania donovani, first emerged and crossed the species barrier in eastern Sudan possibly
around 3040- kYBP.(4) The general dictum of host parasite coevolution is that parasites become less virulent
the more they coexist with their host. Nilo-Saharan speakers were shown in independent genetic analysis to
be the oldest inhabitants of the Sudan and the most ancestral populations. Then what is the explanation for
the fact that the Jum Jum and the situation in southern Sudan and Rahad River that they fell easy prey to VL?
Explanations could be sought within the realms of population genetics and genetic epidemiology
in both cases. Both groups might possess higher frequencies of VL susceptibility alleles.
The severity of the VL epidemic among the Nuer and JumJum could be speculated in the light of these
groups being naive to the parasite i.e. moving recently into the endemic Upper Nile and Blue Nile areas and
progressively encountering the peripheral transmission of the disease sylvatic cycle as more forest areas are
being cleared and inhabited by migrant populations. Oral tradition and archaeological evidence suggests
migration of the Nilotic groups into the area from further north in the past few millennia. The gravity and
high death toll among particular ethnic groups could be interpreted in the light of genetic drift (see below).
The force of drift operates more effectively in situations of isolation or inbreeding hence leading to lower
effective population size (Ne) and excess susceptibility/resistance alleles that may end in the tragic situation
described earlier. The scene of the VL investigation in the Rahad River centred on Koka and Um-Salala