ArticleRoyal Society open science2024
Modelling COVID-19 mutant dynamics: understanding the interplay between viral evolution and disease transmission dynamics.
Article in Royal Society open science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Mechanics of pandemics.EClinicalMedicine · 2026Review
- Modelling COVID-19 mutant dynamics: understanding the interplay between viral evolution and disease transmission dynamics.Royal Society open science · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding virus mutations is critical for shaping public health interventions. These mutations lead to complex multi-strain dynamics often under-represented in models. Aiming to understand the factors influencing variants' fitness and evolution, we explore several scenarios of virus spreading to gain qualitative insight into the factors dictating which variants ultimately predominate at the population level. To this end, we propose a two-strain stochastic model that accounts for asymptomatic transmission, mutations and the possibility of disease import. We find that variants with milder symptoms are likely to spread faster than those with severe symptoms. This is because severe variants can prompt affected individuals to seek medical help earlier, potentially leading to quicker identification and isolation of cases. However, milder or asymptomatic cases may spread more widely, making it harder to control the spread. Therefore, increased transmissibility of milder variants can still result in higher hospitalizations and fatalities due to widespread infection. The proposed model highlights the interplay between viral evolution and transmission dynamics. Offering a nuanced view of factors influencing variant spread, the model provides a foundation for further investigation into mitigating strategies and public health interventions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.