Under the isolation-by-distance model, the strength of spatial genetic structure (SGS) depends on seed and pollen dispersal and genetic drift, which in turn depends on local demographic structure. SGS can also be influenced by historical events such as admixture of differentiated gene pools. We analysed the fine-scale SGS in six populations of a pioneer tree species endemic to Central Africa, Aucoumea klaineana. To infer the impacts of limited gene dispersal, population history and habitat fragmentation on isolation by distance, we followed a stepwise approach consisting of a Bayesian clustering method to detect differentiated gene pools followed by the analysis of kinship-distance curves. Interestingly, despite considerable variation in density, the five populations situated under continuous forest cover displayed very similar extent of SGS. This is likely due to an increase in dispersal distance with decreased tree density. Admixture between two gene pools was detected in one of these five populations creating a distinctive pattern of SGS. In the last population sampled in open habitat, the genetic diversity was in the same range as in the other populations despite a recent habitat fragmentation. This result may due to the increase of gene dispersal compensating the effect of the disturbance as suggested by the reduced extent of SGS estimated in this population. Thus, in A. klaineana, the balance between drift and dispersal may facilitate the maintenance of genetic diversity. Finally, from the strength of the SGS and population density, an indirect estimate of gene dispersal distances was obtained for one site: the quadratic mean parent-offspring distance, sigma(g), ranged between 210 m and 570 m.

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Several studies have focused their attention on the relationship between host genetic factors and susceptibility/resistance to severe malaria. However, there is a paucity of information concerning the role of host genetic factors in asymptomatic malaria, a form of low-grade Plasmodium falciparum infection without clinical symptoms. We investigated in this study the potential relationship between the host (human) genetic polymorphisms (glucose-6-phosphate dehydrogenase [G6PD], mannose binding lectin [MBL], tumor necrosis factor ␣ [TNF␣] −308 and-238 , and nitric oxide synthase 2 [NOS2]-954) and the prevalence and profile of asymptomatic P. falciparum infection in 158 Gabonese schoolchildren. We found that G6PD Aheterozygous females (18 of 74) have a low prevalence of asymptomatic malaria (38.9% versus 67.3%; P ‫ס‬ 0.03, by chi-square test). Children heterozygous for TNF␣-238 (25 of 156) carry high number of diverse infecting parasite genotypes (2.5 versus 1.99; variance F ‫ס‬ 3.05). No statistically significant association was found between MBL, TNF␣-308 , or NOS2 polymorphisms and asymptomatic malaria. Upon combining our data on asymptomatic forms with those from the literature for others forms, we conclude that G6PD Aheterozygous females are protected against all forms of P. falciparum malaria, and that the TNF␣-238A allele confers protection against clinical malaria.

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Mannose-binding lectin (MBL) plays an important role in the early stages of primary infections and during the decay of maternal antibodies in infants. Various studies have looked at the relation between serum MBL concentrations, MBL gene alterations and susceptibility to infections. We investigated the distribution of variant MBL alleles in 626 unrelated adults from sub-Saharan African countries and looked for a potential relation between these alleles and the incidence, prevalence and death rate of tuberculosis for sub-Saharan Africa. We also evaluated the relation between MBL genotypes and susceptibility to HIV-1 infection in 188 Gabonese adults. We found that (i) the prevalence of the common variant MBL alleles is correlated with the incidence of tuberculosis in sub-Saharan Africa (r ¼ 0.565), (ii) the mutant MBL G57E allele, in either the homozygous or compound heterozygous state, is associated with susceptibility to HIV-1 infection in the Gabonese population (P ¼ 0.019).Our data plus those in the literature suggest that individuals who are homozygous for the mutant MBL alleles display increased susceptibility to infections. Interestingly, we found that individuals who are heterozygous for MBL mutations are much less susceptible to infections than those who are homozygous for the wild-type MBL allele.