ArticleJournal of mathematical biology2015
Mathematical model of multivalent virus-antibody complex formation in humans following acute and chronic HIV infections.
Article in Journal of mathematical biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 9 citations in OpenAlex.
- Understanding antibody magnitude and durability following vaccination against SARS-CoV-2.Mathematical biosciences · 2024Article
- Mathematical Modeling of Virus-Mediated Syncytia Formation: Past Successes and Future Directions.Results and problems in cell differentiation · 2024Review
- A Bistable Switch in Virus Dynamics Can Explain the Differences in Disease Outcome Following SIV Infections in Rhesus Macaques.Frontiers in microbiology · 2018Article
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Authors and funding
1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Antibodies that bind viral surface proteins can limit the spread of the infection through neutralizing and non-neutralizing functions. During both acute and chronic Human Immunodeficiency Virus infection, antibody-virion immune complexes are formed, but fail to ensure protection. In this study, we develop a mathematical model of multivalent antibody binding and use it to determine the dynamical interactions that lead to immune complexes formation and the role of complexes with increased numbers of bound antibodies in the pathogenesis of the disease. We compare our predictions with published temporal virus and immune complex data from acute infected patients. Finally, we derive quantitative and qualitative conditions needed for antibody-induced protection.
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