ArticlePLoS computational biology2011
Transmission selects for HIV-1 strains of intermediate virulence: a modelling approach.
Article in PLoS computational biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Phylogenetics and molecular evolution to understand and curb the HIV pandemic.Nature reviews. Microbiology · 2026Review
- Evolution of HIV virulence in response to disease-modifying vaccines: A modeling study.Vaccine · 2023Article
- Evolution of the Envelope Glycoprotein of HIV-1 Clade B toward Higher Infectious Properties over the Course of the Epidemic.Journal of virology · 2019Article
- Estimating the impact of antiretroviral treatment on adult mortality trends in South Africa: A mathematical modelling study.PLoS medicine · 2017Article
- Viral genetic variation accounts for a third of variability in HIV-1 set-point viral load in Europe.PLoS biology · 2017Article
- Effects of contact structure on the transient evolution of HIV virulence.PLoS computational biology · 2017Article
- Modelling the evolution of HIV-1 virulence in response to imperfect therapy and prophylaxis.Evolutionary applications · 2017Article
- Effect of the Latent Reservoir on the Evolution of HIV at the Within- and Between-Host Levels.PLoS computational biology · 2017Article
- A transmission-virulence evolutionary trade-off explains attenuation of HIV-1 in Uganda.eLife · 2016Article
- Evolution of HIV virulence in response to widespread scale up of antiretroviral therapy: a modeling study.Virus evolution · 2016Article
- Conflicting Selection Pressures Will Constrain Viral Escape from Interfering Particles: Principles for Designing Resistance-Proof Antivirals.PLoS computational biology · 2016Article
- High heritability is compatible with the broad distribution of set point viral load in HIV carriers.PLoS pathogens · 2015Article
- HIV competition dynamics over sexual networks: first comer advantage conserves founder effects.PLoS computational biology · 2015Article
- Immuno-epidemiological modeling of HIV-1 predicts high heritability of the set-point virus load, while selection for CTL escape dominates virulence evolution.PLoS computational biology · 2014Article
- An HIV epidemic model based on viral load dynamics: value in assessing empirical trends in HIV virulence and community viral load.PLoS computational biology · 2014Article
- Is HIV short-sighted? Insights from a multistrain nested model.Evolution; international journal of organic evolution · 2013Article
- How effectively can HIV phylogenies be used to measure heritability?Evolution, medicine, and public health · 2013Article
- Inferring the source of transmission with phylogenetic data.PLoS computational biology · 2013Article
- A stochastic multi-scale model of HIV-1 transmission for decision-making: application to a MSM population.PloS one · 2013Article
- Viral phylodynamics.PLoS computational biology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent data shows that HIV-1 is characterised by variation in viral virulence factors that is heritable between infections, which suggests that viral virulence can be naturally selected at the population level. A trade-off between transmissibility and duration of infection appears to favour viruses of intermediate virulence. We developed a mathematical model to simulate the dynamics of putative viral genotypes that differ in their virulence. As a proxy for virulence, we use set-point viral load (SPVL), which is the steady density of viral particles in blood during asymptomatic infection. Mutation, the dependency of survival and transmissibility on SPVL, and host effects were incorporated into the model. The model was fitted to data to estimate unknown parameters, and was found to fit existing data well. The maximum likelihood estimates of the parameters produced a model in which SPVL converged from any initial conditions to observed values within 100-150 years of first emergence of HIV-1. We estimated the 1) host effect and 2) the extent to which the viral virulence genotype mutates from one infection to the next, and found a trade-off between these two parameters in explaining the variation in SPVL. The model confirms that evolution of virulence towards intermediate levels is sufficiently rapid for it to have happened in the early stages of the HIV epidemic, and confirms that existing viral loads are nearly optimal given the assumed constraints on evolution. The model provides a useful framework under which to examine the future evolution of HIV-1 virulence.
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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.