ArticlePLoS computational biology2014
Immuno-epidemiological modeling of HIV-1 predicts high heritability of the set-point virus load, while selection for CTL escape dominates virulence evolution.
Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Attenuation of HIV severity by slightly deleterious mutations can explain the long-term trajectory of virulence evolution.PLoS computational biology · 2025Article
- The genetic architecture of HIV-1 virulence.Virus evolution · 2025Article
- Cross-generational mechanisms of maternal gut microbiota in modulating offspring autism spectrum disorder risk: from the gut-brain axis to translational challenges in precision interventions.Frontiers in aging neuroscience · 2025Review
- Reconstructing multi-strain pathogen interactions from cross-sectional survey data via statistical network inference.Journal of the Royal Society, Interface · 2023Article
- Key Factors and Parameter Ranges for Immune Control of Equine Infectious Anemia Virus Infection.Viruses · 2023Article
- Patient characteristics and determinants of CD4 at diagnosis of HIV in Mexico from 2008 to 2017: a 10-year population-based study.AIDS research and therapy · 2021Article
- Natural selection favoring more transmissible HIV detected in United States molecular transmission network.Nature communications · 2019Article
- Linked within-host and between-host models and data for infectious diseases: a systematic review.PeerJ · 2019Article
- Evolution of HIV-1 within untreated individuals and at the population scale in Uganda.PLoS pathogens · 2018Article
- Dissecting HIV Virulence: Heritability of Setpoint Viral Load, CD4+ T-Cell Decline, and Per-Parasite Pathogenicity.Molecular biology and evolution · 2018Article
- How Germinal Centers Evolve Broadly Neutralizing Antibodies: the Breadth of the Follicular Helper T Cell Response.Journal of virology · 2017Article
- Viral genetic variation accounts for a third of variability in HIV-1 set-point viral load in Europe.PLoS biology · 2017Article
- Estimating the Respective Contributions of Human and Viral Genetic Variation to HIV Control.PLoS computational biology · 2017Article
- Effect of the Latent Reservoir on the Evolution of HIV at the Within- and Between-Host Levels.PLoS computational biology · 2017Article
- Impact of pre-adapted HIV transmission.Nature medicine · 2016Article
- A trend towards increasing viral load in newly diagnosed HIV-infected inpatients in southeast China.Epidemiology and infection · 2016Article
- The impact of antiretroviral therapy on population-level virulence evolution of HIV-1.Journal of the Royal Society, Interface · 2015Article
- The impact of host genetic variation on infection with HIV-1.Nature immunology · 2015Review
- Reply to Jefferys: Declining HIV virulence.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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3 authors.
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Abstract
It has been suggested that HIV-1 has evolved its set-point virus load to be optimized for transmission. Previous epidemiological models and studies into the heritability of set-point virus load confirm that this mode of adaptation within the human population is feasible. However, during the many cycles of replication between infection of a host and transmission to the next host, HIV-1 is under selection for escape from immune responses, and not transmission. Here we investigate with computational and mathematical models how these two levels of selection, within-host and between-host, are intertwined. We find that when the rate of immune escape is comparable to what has been observed in patients, immune selection within hosts is dominant over selection for transmission. Surprisingly, we do find high values for set-point virus load heritability, and argue that high heritability estimates can be caused by the 'footprints' left by differing hosts' immune systems on the virus.
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