Abstract
Evolution is based on mutation processes and the subsequent selection of the best-adapted individuals, i.e., “survival of the fittest”. Thus, diversity is a common feature in living things. Pathogens and their hosts, as well as tumoral processes are no exception. Changes in the genetic material of microorganisms allow them to colonize new ecological niches while hosts try to adapt to the new residents by either eliminating them or by establishing mutualistic interactions. The permanent coexistence of microorganisms and their hosts leads to continuous evolvement necessary for their survival, following a strategy that was initially proposed for coevolution models in predator-prey interactions known as the “Red Queen Hypothesis”. Similar conclusions can be established for tumoral processes. Thus, in general, tumors, microorganisms, and hosts can be considered at the population level as complex distributions of related although not identical individuals. Initially, these complex systems were described in a theoretical model that tried to explain the functioning of populations of primitive replicons during the origin of life. This theory was later experimentally confirmed by analyzing populations of positive-strand RNA viruses or RNA(+). In both cases, for replicons and RNA(+) viruses, the populations are described as quasispecies. Here, we will review the most recent discoveries regarding interactions between population diversity and pathogenicity, both in microorganisms and tumors.
Keywords: Quasispecies, virus, cancer, Tumor, Pathogens, microorganisms, positive-strand RNA, nucleic acid, nucleotide, Red Queen Hypothesis, Muller's ratchet, Q bacteriophage, foot-and-mouth disease, prokaryotes, eukaryotes, human immunodeficiency virus, hepatitis C virus, HIV, reverse transcriptase, lymphocytic choriomeningitis virus, highly active antiretroviral therapy, HAART, metastasis, human oncogenes, Cellular DNA, mutation, heterogeneity, HAACT, Darwinian model, Pseudomonas aeruginosa, Pf4 bacteriophage
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