ArticlePLoS computational biology2021
Why are viral genomes so fragile? The bottleneck hypothesis.
Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Concepts of RNA virus evolution for the design of better antiviral countermeasures.Nature reviews. Microbiology · 2026Review
- Contrasting Effects of Tagging Turnip Mosaic Virus Proteins.Pathogens (Basel, Switzerland) · 2026Article
- Morphological appearance of the B.1.1.7 mutation of the novel coronavirus 2 (SARS-CoV-2) in chest CT.Quantitative imaging in medicine and surgery · 2023Article
- Determinants of Virus Variation, Evolution, and Host Adaptation.Pathogens (Basel, Switzerland) · 2022Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
If they undergo new mutations at each replication cycle, why are RNA viral genomes so fragile, with most mutations being either strongly deleterious or lethal? Here we provide theoretical and numerical evidence for the hypothesis that genetic fragility is partly an evolutionary response to the multiple population bottlenecks experienced by viral populations at various stages of their life cycles. Modelling within-host viral populations as multi-type branching processes, we show that mutational fragility lowers the rate at which Muller's ratchet clicks and increases the survival probability through multiple bottlenecks. In the context of a susceptible-exposed-infectious-recovered epidemiological model, we find that the attack rate of fragile viral strains can exceed that of more robust strains, particularly at low infectivities and high mutation rates. Our findings highlight the importance of demographic events such as transmission bottlenecks in shaping the genetic architecture of viral pathogens.
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