PROTECTION AGAINST MALARIA BY THALASSEMIA AND HEMOGLOBIN-VARIANTS

Recent epidemiological evidence has given increasing support to Haldan e's 1949 hypothesis that heterozygotes for such genetic disorders as t halassaemia might be protected against malaria, hence explaining the h igh gene frequencies for such disorders in endemic areas. As discussed here by Yongyuth Yuthavong and Prapon Wilairat, the possible cellular mechanisms, although still unclear, are emerging from in vitro studie s which increasingly point to the importance of immune clearance mecha nisms in some cases (such as alpha-thalassaemia and haemoglobin E). In other situations, decreased survival of the intra-erythrocytic parasi te or decreased parasite invasion of the variant red blood cells may e xplain the protective effect. Whatever the cellular mechanisms are, th e ultimate decisive factor is the relative fitness of the infected var iant host, which may not be simply extrapolated from the cellular stud ies.