Xeroderma pigmentosum, defective DNA repair--and schistosomiasis?

Xeroderma pigmentosum (XP) is more common in Japan and Egypt than in Europe and America. Some unidentified selective advantage for the carrier of an XP gene is the probable explanation for these regional increases. The question then arises as to what unusual environmental factor(s) Japan and Egypt, otherwise so disparate, might share that is not shared by most of the Western World. The dependence on flooded lands for crop production is one such feature, and human schistosomiasis has been a consequence in both places. The second question becomes, therefore, how might this parasitism be responsible for an increased frequency of XP genes? Schistosomal cercariae, being phototropic, may be assumed to suffer considerable sunlight damage to their DNA immediately before they penetrate the integument of some vertebrate. The hypothesis is advanced that they obtain assistance from their vertebrate host in repairing this damage. Should that be the case, a host less proficient than normal at providing such assistance--as the XP heterozygote might be--, would promote the survival and maturation of relatively few parasites, and thus resist the general debility associated with heavy adult-worm burdens. In a broader sense, the hypothesis suggests that a host can acquire a degree of resistance to a parasite as result of a mutation that affects some essential biochemical mechanism in which the parasite depends on the host for assistance.