From the end of 1994 to the beginning of 1995, 49 patients with hemorrhagic symptoms were hospitalized in the Makokou General Hospital in northeastern Gabon. Yellow fever (YF) virus was first diagnosed in serum by use of polymerase chain reaction followed by blotting, and a vaccination campaign was immediately instituted. The epidemic, known as the fall 1994 epidemic, ended 6 weeks later. However, some aspects of this epidemic were atypical of YF infection, so a retrospective check for other etiologic agents was undertaken. Ebola (EBO) virus was found to be present concomitantly with YF virus in the epidemic. Two other epidemics (spring and fall 1996) occurred in the same province. GP and L genes of EBO virus isolates from all three epidemics were partially sequenced, which showed a difference of õ0.1% in the base pairs. Sequencing also showed that all isolates were very similar to subtype Zaire EBO virus isolates from the Democratic Republic of the Congo.

Several human genetic factors, including red blood cell polymorphisms (ABO blood group, sickle-cell trait, G6PD deficiency) as well as point mutations in the mannose binding protein (MBP) and in the promoter regions of both the TNF-␣ and NOS2 genes, influence the severity of disease due to infection with Plasmodium falciparum. We assessed their impact on mild P. falciparum malaria, as part of a longitudinal investigation of clinical, parasitological and immunological parameters in a cohort of 300 Gabonese schoolchildren. We found the following frequencies: blood group O (0.54), sicklecell trait (0.23), G6PD deficiency (0.09), MBP gene mutations (0.34), TNF-␣ promoter mutations (at positions −238: 0.17 and −308: 0.22) and NOS2 promoter mutation (0.18). Blood group O or hemoglobin AA were associated with protection against higher parasitemia. Girls with normal G6PD enzyme activity were protected against clinical malaria attacks. In addition, we demonstrated for the first time that the mutation at position −238 of the gene coding for the promoter region of TNF-␣ was positively correlated with the level of the antibody response specific for epitopes of the antigens MSA-2 and RAP-1 of P. falciparum. Genes and Immunity (2000) 1, 435-441.

Abstract. An exhaustive epidemiologic and serologic survey was carried out in five gold-panning villages situated in northeastern Gabon to estimate the degree of exposure of to leptospirosis and Ebola virus. The seroprevalence was 15.7% for leptospirosis and 10.2% for Ebola virus. Sixty years after the last seroepidemiologic survey of leptospirosis in Gabon, this study demonstrates the persistence of this infection among the endemic population and the need to consider it as a potential cause of hemorrhagic fever in Gabon. There was no significant statistical correlation between the serologic status of populations exposed to both infectious agents, indicating the lack of common risk factors for these diseases.

Abstract. A treatment-reinfection study design was used to investigate the relationships between host immunologic and/or genetic factors and resistance to reinfection with Plasmodium falciparum. Sixty-one children in Gabon were enrolled in a cross-sectional study to measure the prevalence of each human plasmodial species. All were given amodiaquine for radical cure of parasites, and 40 were subsequently followed-up for 30 weeks. Successive blood smears were examined to measure the delay of reappearance in blood of asexual stages of P. falciparum parasites. Presence of infection during the cross-sectional survey was associated with male sex, non-deficient glucose-6-phosphate dehydrogenase activity, plasma interleukin-10 level, and anti-LSA-Rep antibody concentration. Resistance to reinfection was related to the presence of anti-LSA-J antibodies, and the absence of anti-LSA-Rep antibodies. Moreover, P. malariae-infected subjects were usually co-infected with P. falciparum, and were also more rapidly reinfected with P. falciparum after treatment, compared with those without P. malariae infection.Most studies aimed to investigate the protection against Plasmodium falciparum malaria have used malaria attacks as criteria.1,2 However, these criteria require long and precise follow-up of the populations because malaria attacks occur rarely, even in hyperendemic areas where children who present more than 2 malaria attacks per year are rare. 3 Moreover, such criteria mainly investigate protection against blood stages of the parasite and do not allow the assessment of protection against the pre-erythrocytic stages. The existence of such protection is shown by the fact that only a small proportion part of infective bites leads to the appearance of parasites in the peripheral blood. 4 Similarly, the prevalence rates of blood parasite infections following antimalarial treatment are extremely lower than presumed in view of the number of infective bites from mosquitoes. 5 In this context, effector mechanisms may be directed against the sporozoites, the liver stages, or both. Protection against the sporozoites may result from a specific humoral response because it has been demonstrated for the antibody directed to the repetitive epitope (NANP) 3 from the circumsporozoite (CS) protein. 6 Antibody targeted against liver-stage antigens may also contribute to the reduction of the emergence of P. falciparum from the liver. The plasma levels of Th1-type and Th2-type cytokines are also thought to play a major role in individual levels of protection. To evaluate the level of protection against the sporozoite and liver stages of the parasite, we first performed a cross-sectional study to assess the parasitologic status of children living in Gabon, an area hyperendemic for malaria. All children then received a curative antimalarial treatment and were enrolled in a longitudinal follow-up to measure their delay of reinfection by natural challenge. Relationships between the immunologic factors and the infection rate at the beginning of the s...