ArticleProceedings of the National Academy of Sciences of the United States of America2025
A binary trait model reveals the fitness effects of HIV-1 escape from T cell responses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Linkage-aware inference of fitness from short-read time-series genomic data.bioRxiv : the preprint server for biology · 2026Article
- Chronic infections can generate SARS-CoV-2-like bursts of viral evolution without epistasis.Virus evolution · 2026Article
- Linkage-aware inference of fitness from short-read time-series genomic data.Virus evolution · 2026Article
- Selection Estimation from Genetic Time-Series Data: Effects of Limited Sampling and Genetic Drift.Molecular biology and evolution · 2025Article
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- Back-projection improves inference from sparsely sampled genomic surveillance data.bioRxiv : the preprint server for biology · 2025Article
- Inferring fitness seascapes from evolutionary histories.bioRxiv : the preprint server for biology · 2025Article
- A binary trait model reveals the fitness effects of HIV-1 escape from T cell responses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Efficient epistasis inference via higher-order covariance matrix factorization.bioRxiv : the preprint server for biology · 2024Article
- Chronic infections can generate SARS-CoV-2-like bursts of viral evolution without epistasis.bioRxiv : the preprint server for biology · 2024Article
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Abstract
Natural selection often acts on multiple traits simultaneously. For example, the virus HIV-1 faces pressure to evade host immunity while also preserving replicative fitness. While past work has studied selection during HIV-1 evolution, as in other examples where selection acts on multiple traits, it is challenging to quantitatively separate different contributions to fitness. This task is made more difficult because a single mutation can affect both immune escape and replication. Here, we develop an evolutionary model that disentangles the effects of escaping CD8
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