ArticleMolecular systems biology2010
Intracellular transactivation of HIV can account for the decelerating decay of virus load during drug therapy.
Article in Molecular systems biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 88 citations in OpenAlex.
- Variation of TNF modulates cellular immunity of gregarious and solitary locusts against fungal pathogenProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Pre-existing resistance in the latent reservoir can compromise VRC01 therapy during chronic HIV-1 infection.PLoS computational biology · 2020Article
- Probabilistic control of HIV latency and transactivation by the Tat gene circuit.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Trade-off between synergy and efficacy in combinations of HIV-1 latency-reversing agents.PLoS computational biology · 2018Article
- A multi-scale mathematical modeling framework to investigate anti-viral therapeutic opportunities in targeting HIV-1 accessory proteins.Journal of theoretical biology · 2015Article
- Quantifying the Antiviral Effect of IFN on HIV-1 Replication in Cell Culture.Scientific reports · 2015Article
- Quantifying the turnover of transcriptional subclasses of HIV-1-infected cells.PLoS computational biology · 2014Article
- Intracellular dynamics of HIV infection.Journal of virology · 2014Article
- Quantification of viral infection dynamics in animal experiments.Frontiers in microbiology · 2013Review
- Modeling the within-host dynamics of HIV infection.BMC biology · 2013Review
- Contribution of follicular dendritic cells to persistent HIV viremia.Journal of virology · 2013Article
- Impaired immune evasion in HIV through intracellular delays and multiple infection of cells.Proceedings. Biological sciences · 2012Article
- Latency profiles of full length HIV-1 molecular clone variants with a subtype specific promoter.Retrovirology · 2011Article
- Implications of CTL-mediated killing of HIV-infected cells during the non-productive stage of infection.PloS one · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basic virus dynamics models have been essential in understanding quantitative issues of HIV replication. However, several parts of the viral life cycle remain elusive. One of the most critical steps is the start of viral transcription, which is governed by the regulatory protein trans-activator of transcription (Tat) that induces a positive feedback loop. It has been shown that this feedback loop can alternate between two states leading to a transient activation of viral transcription. Using Monte Carlo simulations, we integrate the transactivation circuit into a new virus dynamics model having an age-dependent transactivation rate and reversion into latency. The cycling of infected cells between an activated and latent state results in the typical decelerating decay of virus load following therapy. Further, we hypothesize that the activation of latently infected cells is governed by the basal transcription rate of the integrated provirus rather than the intra- or extracellular environment. Finally, our systems approach to modeling virus dynamics offers a promising framework to infer the extracellular dynamics of cell populations from their intracellular reaction networks.
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