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Evaluation of the Efficacy And Toxicity of RNAs Targeting HIV-1 Production for Use in Gene or Drug Therapy
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Increased T cell trafficking as adjunct therapy for HIV-1.
Helen R Fryer1, Steven M Wolinsky2, Angela R McLean1
1Institute for Emerging Infections, Department of Zoology, University of Oxford, The Peter Medawar Building for Pathogen Research, South Parks Road, Oxford, United Kingdom.
Plos Computational Biology
|March 3, 2018
Summary
Antiretroviral therapy suppresses HIV-1 but does not eliminate viral reservoirs. A new strategy aims to reduce viral replication in sanctuary sites, potentially contributing to a functional cure for HIV-1.
Area of Science:
- Virology
- Immunology
- Mathematical Biology
Background:
- Antiretroviral therapy (ART) suppresses human immunodeficiency virus-type 1 (HIV-1) to undetectable levels.
- Replication-competent HIV-1 reservoirs persist despite ART, leading to viral rebound upon treatment cessation.
- Current strategies targeting HIV-1 reservoirs have shown limited success.
Purpose of the Study:
- To propose a novel mathematical model for eliminating HIV-1 reservoirs.
- To investigate a new approach targeting persistent viral replication in drug sanctuaries.
- To explore strategies for achieving a functional cure for HIV-1 infection.
Main Methods:
- Development of a mathematical model to simulate HIV-1 dynamics.
- Analysis of viral replication in drug sanctuary sites.
- Modeling the impact of CD4 T cell trafficking modulation.
Main Results:
- Persistent viral replication in drug sanctuaries contributes to HIV-1 reservoir maintenance.
- Reducing CD4 T cell residency time in sanctuaries can disrupt viral replication.
- Mathematical modeling suggests this approach can render ongoing replication unsustainable.
Conclusions:
- A strategy to reduce CD4 T cell residency time in drug sanctuaries is proposed.
- This approach, combined with ART, may target persistent HIV-1 replication.
- Orchestrating CD4 T cell trafficking could be a key component of a functional HIV-1 cure.
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