A viral quasispecies is a population structure of viruses with a large number of variant genomes (related by mutations). Quasispecies result from high mutation rates as mutants arise continually and change in relative frequency as viral replication and selection proceeds.[1]
The theory predicts that a viral quasispecies at a low but evolutionarily neutral and highly connected (that is, flat) region in the fitness landscape will outcompete a quasispecies located at a higher but narrower fitness peak in which the surrounding mutants are unfit.[2][3] This phenomenon has been called 'the quasispecies effect' or, more recently, the 'survival of the flattest'.[4]
The term quasispecies was adopted from a theory of the origin of life in which primitive replicons consisted of mutant distributions, as found experimentally with present-day RNA viruses within their host.[5][6] The theory provided a new definition of wild type when describing viruses, and a conceptual framework for a deeper understanding of the adaptive potential of RNA viruses than is offered by classical studies based on simplified consensus sequences.[1]
The quasispecies model is most applicable when the genome size is limited and the mutation rate is high, and so is most relevant to RNA viruses (including important pathogens) because they have high mutation rates (approx one error per round of replication),[7] though the concepts can apply to other biological entities such as reverse transcribing DNA viruses like hepatitis B.[8] In such scenarios, complex distributions of closely related variant genomes are subjected to genetic variation, competition and selection, and may act as a unit of selection. Therefore, the evolutionary trajectory of the viral infection cannot be predicted solely from the characteristics of the fittest sequence. High mutation rates also place an upper limit compatible with inheritable information. Crossing such a limit leads to RNA virus extinction, a transition that is the basis of an antiviral design termed lethal mutagenesis, and of relevance to antiviral medicine.[1]
The relevance of quasispecies in virology has been the subject of extended debate. However, standard clonal analyses and deep sequencing methodologies have confirmed the presence of myriads of mutant genomes in viral populations, and their participation in adaptive processes.[1]
- ^ a b c d Domingo E, García-Crespo C, Perales C (29 September 2021). "Historical Perspective on the Discovery of the Quasispecies Concept". Annual Review of Virology. 8 (1): 51–72. doi:10.1146/annurev-virology-091919-105900. hdl:10261/265663. ISSN 2327-056X. PMID 34586874.
- ^ van Nimwegen E, Crutchfield JP, Huynen M (August 1999). "Neutral evolution of mutational robustness". Proceedings of the National Academy of Sciences of the United States of America. 96 (17): 9716–20. arXiv:adap-org/9903006. Bibcode:1999PNAS...96.9716V. doi:10.1073/pnas.96.17.9716. PMC 22276. PMID 10449760.
- ^ Wilke CO, Wang JL, Ofria C, Lenski RE, Adami C (July 2001). "Evolution of digital organisms at high mutation rates leads to survival of the flattest". Nature. 412 (6844): 331–3. Bibcode:2001Natur.412..331W. doi:10.1038/35085569. PMID 11460163. S2CID 1482925.
- ^ Elena SF, Agudelo-Romero P, Carrasco P, Codoñer FM, Martín S, Torres-Barceló C, Sanjuán R (May 2008). "Experimental evolution of plant RNA viruses". Heredity. 100 (5): 478–83. doi:10.1038/sj.hdy.6801088. PMC 7094686. PMID 18253158.
- ^ Eigen M, McCaskill J, Schuster P (1988). "Molecular Quasi-Species". Journal of Physical Chemistry. 92 (24): 6881–6891. doi:10.1021/j100335a010. hdl:11858/00-001M-0000-002C-84A7-C. S2CID 96727272.
- ^ Nowak MA (April 1992). "What is a quasispecies?". Trends in Ecology & Evolution. 7 (4): 118–21. doi:10.1016/0169-5347(92)90145-2. PMID 21235976.
- ^ Drake JW, Holland JJ (November 1999). "Mutation rates among RNA viruses". Proceedings of the National Academy of Sciences of the United States of America. 96 (24): 13910–3. Bibcode:1999PNAS...9613910D. doi:10.1073/pnas.96.24.13910. PMC 24164. PMID 10570172.
- ^ Le Clercq LS (2014-06-18). Molecular characterization of full genome hepatitis b virus sequences from an urban hospital cohort in Pretoria, South Africa. Pretoria, South Africa: University of Pretoria. OCLC 958495192.