[Malaria, genetics and molecular biology: myths, hopes and realities].

In the last two decades, progress in molecular biology has revealed a considerable genetic diversity among several parasitic species and especially in Plasmodium falciparum. This variability is of course facilitated by the haploid state of all plasmodial stages present in the human organism. Demonstrating this has lead to great progress in understanding some of the great epidemiological, pathophysiological, or therapeutic problems raised by malaria. The therapeutic aspects, especially those concerning resistance to antimalarials, will be presented elsewhere. We will deal only the following questions Several studies, some of which are very recent, partially answer these questions and our expertise should considerably increase with the future full sequencing of the Plasmodium falciparum genome. These observations are of considerable interest but should not be over estimated. Indeed, the structure of a genome does not reflect all the aspects of biological reality and it will be long and difficult to establish a correspondence between plasmodial genotypes and the features of a parasitic disease for which there is no true experimental model. Furthermore, the host-parasite relationships are of course not unifactorial and do not limit themselves to the parasite's features. Ecological and ethiological parameters, as well as the anophele's vector capacity, the human genetic predisposition for receptivity or sensitivity to malaria, and specific or non-specific immune phenomena all play a role. Possible interactions with co-infecting micro-organisms, whether viruses (CMV, HIV), or other parasites of the same genus (Plasmodiumvivax), or even other strains of the same parasitic species (Plasmodium falciparum) may also be of crucial importance