Abstract
Infection of an organism or cells in culture with a single infectious genome of an RNA virus results in the prompt formation of a spectrum of mutants, as has been experimentally documented with representatives of the major groups of RNA virus pathogens.1 This fact is critical for the understanding of viral pathogenesis, since it means that a virus does not exist as a genetically defined entity but rather as a distribution of genomes which differ from each other in one or several positions in their nucleotide sequence (figure 1). Some of these closely related but non-identical genomes may have biological properties which differ from those of the average viral population or from those of other components of the mutant spectrum. Thus, genetic heterogeneity is paralleled by a phenotypic heterogeneity in viral populations. Well documented examples are the presence in mutant spectra of variants with altered antigenicity, host cell tropism, capacity to induce interferon, decreased sensitivity to antiviral inhibitors, or variants which display altered patterns of viral gene expression (specific examples and reviews in refs. 2-13).
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Domingo, E. et al. (2003). Detection and Biological Implications of Genetic Memory in Viral Quasispecies. In: Matsumori, A. (eds) Cardiomyopathies and Heart Failure. Developments in Cardiovascular Medicine, vol 248. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9264-2_21
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DOI: https://doi.org/10.1007/978-1-4419-9264-2_21
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