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Synopsis Viral evolution unfolds across nested layers of adaptation, much like a set of Matryoshka dolls. The outermost, well-studied layer involves interactions between viruses and their hosts—where immune evasion, cross-species transmission, and long-term coevolution drive viral diversification. Yet, hidden within this framework is an often-overlooked inner layer: the coevolution of viruses with their own molecular parasites, defective interfering (DI) particles, and defective viral genomes (DVGs). These molecular parasites exploit viral replication machinery, reshaping infection dynamics and imposing selective pressures that influence viral fitness, transmission, and persistence. This perspective synthesizes evidence from experimental evolution, mathematical modeling, and molecular virology to propose a more integrated view of viral evolution. By framing host–virus interactions and virus-DI particle dynamics within a unified evolutionary framework, we highlight the underappreciated role of DI particles as evolutionary players, not just aberrant byproducts. Recognizing these internal layers of viral evolution may inform the development of antiviral strategies and broader questions in host–pathogen coevolution.
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Host Competitive Asymmetries Accelerate Viral Evolution in a Microbe–Virus Coevolutionary System
ABSTRACT Microbial host populations evolve traits conferring specific resistance to viral predators via various defence mechanisms, while viruses reciprocally evolve traits to evade these defences. Such coevolutionary dynamics often involve diversification promoted by negative frequency‐dependent selection. However, microbial traits conferring competitive asymmetries can induce directional selection, opposing diversification. Despite extensive research on microbe–virus coevolution, the combined effect of both host trait types and associated selection remains unclear. Using a CRISPR‐mediated coevolutionary system, we examine how the co‐occurrence of both trait types impacts viral evolution and persistence, previously shown to be transient and nonstationary in computational models. A stochastic model incorporating host competitive asymmetries via variation of intrinsic growth rates reveals that competitively advantaged host clades generate the majority of immune diversity. Greater asymmetries extend viral extinction times, accelerate viral adaptation locally in time and augment long‐term local adaptation. These findings align with previous experiments and provide further insights into long‐term coevolutionary dynamics.
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- Award ID(s):
- 2022049
- PAR ID:
- 10607989
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- Ecology Letters
- Volume:
- 28
- Issue:
- 6
- ISSN:
- 1461-023X
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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