[en] Full text: Microbial infections are highly dynamic processes in which the invading pathogen must counteract host responses to complete an infectious cycle. Viruses offer a broad repertoire of strategies to cope with host defences. Complex DNA viruses encode a number of immunomodulatory proteins aimed at interacting with the host to modulate host responses. In contrast with this 'interacting' strategy, the highly variable RNA viruses employ an 'evasion' strategy, with the frequent selection of mutants capable of evading host immune responses. Mutation rates for RNA viruses are in the range of 10-3 to 10-5 misincorporations per nucleotide copied. This continuous mutational input has as a result that viral genome populations do not consist of a defined nucleotide sequence but of multitudes of closely related sequences. The entire mutant distribution is termed a viral quasispecies. The spectrum of mutants serves as a reservoir of genetic and phenotypic variants. The continuous replenishment of this dynamic reservoir constitutes an adaptative strategy for RNA viruses since selective pressures can result in dominance of viral subpopulations that were a minority in the parental distribution of mutants. Quasispecies adaptability is reflected not only in evasion of immune responses but also in changes in cell tropism and host range of viruses, with implications for viral disease emergence and re-emergence. Several examples of human and animal viruses in which quasispecies dynamics plays a role in viral persistence and disease progression will be discussed. Quasispecies dynamics has additional implications for virus evolution, the diagnosis of viral disease and the design of preventive and therapeutic strategies. Viral populations can contain a memory of those genomes that were dominant at an earlier stage of their evolutionary history. This is a genetic memory in the form of minority components of the mutant spectrum, first described with two independent lineages of foot-and-mouth disease virus (FMDV) in cell culture. Memory has been recently described for human inmunodeficiency virus type 1 (HIV- 1) in vivo. The identification of such memory genomes may be relevant for viral diagnosis during chronic infectious, to avoid rapid selection of mutants present at memory levels (for example in the face of a modification of treatment during HIV infections). Regarding prevention, quasispecies dynamics requires administration of multivalent vaccines (consisting of multiple B-and T-cell epitopes and when possible, several different relevant sequences of those same epitopes) to avoid or delay the selection of escape mutants. Regarding therapy, quasispecies dynamics demands combination therapy with multiple antiviral agents directed to independent functional targets of the virus, to avoid or delay selection of inhibitor-escape mutants. An example is highly active antiretroviral therapy (HAART) to control HIV infections. Quasispecies dynamics has opened also the possibility of a new antiviral therapy based on virus entry into error catastrophe, termed lethal mutagenesis. Recent results on these several implications of quasispecies dynamics will be reviewed. These recent developments underline the need of trans-disciplinary approaches (involving evolutionary biology, physics and experimental virology) to the understanding of microbial infections and to the design of appropriate preventive and therapeutic treatments. (author)