ArticleJournal of the Royal Society, Interface2005
HIV recombination: what is the impact on antiretroviral therapy?
Article in Journal of the Royal Society, Interface, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- A general and biomedical perspective of viral quasispecies.RNA (New York, N.Y.) · 2025Review
- Modeling dynamics of acute HIV infection incorporating density-dependent cell death and multiplicity of infection.PLoS computational biology · 2024Article
- Consequences of Genetic Recombination on Protein Folding Stability.Journal of molecular evolution · 2023Article
- Superinfection exclusion: A viral strategy with short-term benefits and long-term drawbacks.PLoS computational biology · 2022Article
- ProteinEvolverABC: coestimation of recombination and substitution rates in protein sequences by approximate Bayesian computation.Bioinformatics (Oxford, England) · 2021Article
- Quantifying the dynamics of viral recombination during free virus and cell-to-cell transmission in HIV-1 infection.Virus evolution · 2021Article
- Effect of synaptic cell-to-cell transmission and recombination on the evolution of double mutants in HIV.Journal of the Royal Society, Interface · 2020Article
- Multiple infection of cells changes the dynamics of basic viral evolutionary processes.Evolution letters · 2019Article
- Pathogen evolution in finite populations: slow and steady spreads the best.Journal of the Royal Society, Interface · 2018Article
- Sanger and Next Generation Sequencing Approaches to Evaluate HIV-1 Virus in Blood Compartments.International journal of environmental research and public health · 2018Article
- The Role of Recombination in Evolutionary Rescue.Genetics · 2016Article
- Clonality and intracellular polyploidy in virus evolution and pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Modeling multiple infection of cells by viruses: Challenges and insights.Mathematical biosciences · 2015Article
- Genetic Consequences of Antiviral Therapy on HIV-1.Computational and mathematical methods in medicine · 2015Review
- Recombination accelerates adaptation on a large-scale empirical fitness landscape in HIV-1.PLoS genetics · 2014Article
- Superinfection with drug-resistant HIV is rare and does not contribute substantially to therapy failure in a large European cohort.BMC infectious diseases · 2013Article
- Modeling sequence evolution in HIV-1 infection with recombination.Journal of theoretical biology · 2013Article
- Virus dynamics in the presence of synaptic transmission.Mathematical biosciences · 2013Article
- Synaptic transmission and the susceptibility of HIV infection to anti-viral drugs.Scientific reports · 2013Article
- Impaired immune evasion in HIV through intracellular delays and multiple infection of cells.Proceedings. Biological sciences · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retroviral recombination is a potential mechanism for the development of multiply drug resistant viral strains but the impact on the clinical outcomes of antiretroviral therapy in HIV-infected patients is unclear. Recombination can favour resistance by combining single-point mutations into a multiply resistant genome but can also hinder resistance by breaking up associations between mutations. Previous analyses, based on population genetic models, have suggested that whether recombination is favoured or hindered depends on the fitness interactions between loci, or epistasis. In this paper, a mathematical model is developed that includes viral dynamics during therapy and shows that population dynamics interact non-trivially with population genetics. The outcome of therapy depends critically on the changes to the frequency of cell co-infection and I review the evidence available. Where recombination does have an effect on therapy, it is always to slow or even halt the emergence of multiply resistant strains. I also find that for patients newly infected with multiply resistant strains, recombination can act to prevent reversion to wild-type virus. The analysis suggests that treatment targeted at multiple parts of the viral life-cycle may be less prone to drug resistance due to the genetic barrier caused by recombination but that, once selected, mutants resistant to such regimens may be better able to persist in the population.
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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.