ArticlePloS one2012
Effect of synaptic transmission on viral fitness in HIV infection.
Article in PloS one, 2012. 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, 34 citations in OpenAlex.
- A hybrid stochastic-deterministic approach to explore multiple infection and evolution in HIV.PLoS computational biology · 2021Article
- Quantifying the dynamics of viral recombination during free virus and cell-to-cell transmission in HIV-1 infection.Virus evolution · 2021Article
- Modeling the role of macrophages in HIV persistence during antiretroviral therapy.Journal of mathematical biology · 2020Article
- 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
- Synaptic transmission may provide an evolutionary benefit to HIV through modulation of latency.Journal of theoretical biology · 2018Article
- The role of spatial heterogeneity in the evolution of local and global infections of viruses.PLoS computational biology · 2018Article
- Modeling Viral Spread.Annual review of virology · 2016Review
- Modeling multiple infection of cells by viruses: Challenges and insights.Mathematical biosciences · 2015Article
- Contribution of HIV-1 genomes that do not integrate to the basic reproductive ratio of the virus.Journal of theoretical biology · 2015Article
- Improving the estimation of the death rate of infected cells from time course data during the acute phase of virus infections: application to acute HIV-1 infection in a humanized mouse model.Theoretical biology & medical modelling · 2014Article
- Virus dynamics in the presence of synaptic transmission.Mathematical biosciences · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
HIV can spread through its target cell population either via cell-free transmission, or by cell-to-cell transmission, presumably through virological synapses. Synaptic transmission entails the transfer of tens to hundreds of viruses per synapse, a fraction of which successfully integrate into the target cell genome. It is currently not understood how synaptic transmission affects viral fitness. Using a mathematical model, we investigate how different synaptic transmission strategies, defined by the number of viruses passed per synapse, influence the basic reproductive ratio of the virus, R(0), and virus load. In the most basic scenario, the model suggests that R(0) is maximized if a single virus particle is transferred per synapse. R(0) decreases and the infection eventually cannot be maintained for larger numbers of transferred viruses, because multiple infection of the same cell wastes viruses that could otherwise enter uninfected cells. To explain the relatively large number of HIV copies transferred per synapse, we consider additional biological assumptions under which an intermediate number of viruses transferred per synapse could maximize R(0). These include an increased burst size in multiply infected cells, the saturation of anti-viral factors upon infection of cells, and rate limiting steps during the process of synapse formation.
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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.