Since we have been discussing lack of immunity of raw fooders to malaria, we
might ask ourselves if there are some genetic factors which protect against it.
Here is the beginning of an answer:

People who lack the ability to produce the enzyme G6PD are resistant to malaria.
On the other hand, lacking that enzyme causes some health problems, like
susceptibility to favism (for people who eat fava beans).

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Blood Rev 1996 Mar;10(1):45-52, G6PD: population genetics and clinical
manifestations, Beutler E

The glucose-6-phosphate dehydrogenase (G6PD) gene is X-linked. There are
numerous mutations that cause a deficiency of this enzyme in erythrocytes.
G6PD deficiency can produce anemia, both when drugs are administered and
under the stress induced by infection. Functionally severe variants cause
hereditary non-spherocytic hemolytic anemia, i.e. anemia even in the
absence of stress. Neonatal jaundice occurs in G6PD deficiency, but it is likely
that it is largely due to impairment of liver function, rather than to
hemolysis. It has been suggested that there are clinical manifestations of G6PD
deficiency that are related to other tissues, but the existence of these is not
well documented. Some mutations that produce G6PD deficiency in red cells exist
at polymorphic frequencies. Individuals with such mutations seem to have
enjoyed a selective advantage because of resistance to falciparum malaria.
Different mutations, each characteristic of certain populations, are found, and
have been characterized at the deoxyribonucleic acid (DNA) level. G6PD
A-(202A376G) is the most common African mutation. G6PD
Mediterranean(563T) is found in Southern Europe, the Middle East and in
the Indian subcontinent. Several other mutations are common in Asia.
Genetic variability of G6PD has played an important role in the
understanding of a variety of developmental processes.

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Southeast Asian J Trop Med Public Health 1991 Jun;22(2):176-182, G6PD deficiency
and fava bean consumption do not produce hemolysis in Thailand, Kitayaporn D,
Charoenlarp P, Pattaraarechachai J, Pholpoti T

Favism, a hemolytic condition associated with fava bean consumption among
the glucose-6-phosphate dehydrogenase (G6PD) deficient persons, is well
described in the Middle East and Mediterranean areas. However, it is not well
documented among the Thais or other Southeast Asians. It is possible that it
does exist but that hemolysis which develops is of very minor degree and thus
escapes clinical detection. This cross-sectional study hypothesizes that if the
fava bean and G6PD deficiency interact in the Thai population, they should
cause a significant difference in hematocrit level. The study was carried out in
a community hospital in a malaria endemic area. We found that there was a
trivial difference of the hematocrit (approximately 1%) which was too small
to warrant any clinical significance after controlling for the extraneous
effects of age, sex, use of malaria chemoprophylaxis, falciparum infection, use
of analgesics/antipyretics and admission status of the patients (p = 0.668).
This may be due to the presence of different G6PD mutants to those found
elsewhere or due to different consumption patterns of fava beans among the
Thais compared to people in other areas with high prevalence of G6PD
deficiency.
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Bioessays 1996 Aug;18(8):631-637, A new lease of life for an old enzyme, Martini
G, Ursini MV

We review here some recent data about glucose-6-phosphate dehydrogenase
(G6PD), the first and key regulatory enzyme of the pentose phosphate
pathway. New evidence has been presented to suggest that malaria is a
selective agent for G6PD deficiency, which is the most common enzymopathy
in man, and that G6PD deficiency, generally considered to be a mild and
benign condition, is significantly disadvantageous in certain environmental
conditions. At the molecular level, the enzyme structure has recently been
elucidated and mechanisms regulating G6PD gene expression have been
determined. A G6PD knock-out mutation introduced in mouse cells makes
them exquisitely sensitive to oxidative stress, indicating that this ubiquitous
metabolic enzyme has a major role in the defence against oxidative stress,
even in eukaryotic nucleated cells, which have several alternative routes for
providing the same protection. Because of the high prevalence of G6PD
deficiency in many populations, it is expected that these findings will prompt
further studies to ascertain the putative role of G6PD deficiency in conditions
such as carcinogenesis and ageing.