ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2023
Inspecting the interaction between human immunodeficiency virus and the immune system through genetic turnover.
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
- Dynamics of memory B cells and plasmablasts in healthy individuals.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interdisciplinary approaches to predicting evolutionary biology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- Inspecting the interaction between human immunodeficiency virus and the immune system through genetic turnover.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic infections of the human immunodeficiency virus (HIV) create a very complex coevolutionary process, where the virus tries to escape the continuously adapting host immune system. Quantitative details of this process are largely unknown and could help in disease treatment and vaccine development. Here we study a longitudinal dataset of ten HIV-infected people, where both the B-cell receptors and the virus are deeply sequenced. We focus on simple measures of turnover, which quantify how much the composition of the viral strains and the immune repertoire change between time points. At the single-patient level, the viral-host turnover rates do not show any statistically significant correlation, however, they correlate if one increases the amount of statistics by aggregating the information across patients. We identify an anti-correlation: large changes in the viral pool composition come with small changes in the B-cell receptor repertoire. This result seems to contradict the naïve expectation that when the virus mutates quickly, the immune repertoire needs to change to keep up. However, a simple model of antagonistically evolving populations can explain this signal. If it is sampled at intervals comparable with the sweep time, one population has had time to sweep while the second cannot start a counter-sweep, leading to the observed anti-correlation. This article is part of the theme issue 'Interdisciplinary approaches to predicting evolutionary biology'.
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