bioRxiv ScienceSearch

bioRxiv · 10.1101/518704

Mean-field computational approach to HIV dynamics on a fitness landscape

Abstract

During acute infection by the human immunodeficiency virus (HIV), the intra-host viral population accumulates mutations due to selection by host T cell responses. The timescales at which HIV mutations emerge vary widely, correlating with their diversity in the global population of hosts, and with the relative strengths at which different regions of the HIV sequence are targeted by the host. In recent years, \"fitness landscapes\" of HIV proteins have been estimated from this global diversity, capturing residue-specific fitness costs and epistatic interactions between residues, and have been shown to predict the locations and relative timescales of escape mutations arising in hosts with known T cell responses. However, existing computational approaches to HIV dynamics that make use of realistic fitness landscapes are limited to fixed-population-size stochastic simulations, and extending other dynamical approaches to capture full sequence-level detail is computationally nontrivial. In this paper, we introduce and study an alternative approach for simulating HIV dynamics given a fitness landscape, which we designate the evolutionary mean-field (EMF) method. EMF is the high-recombination-rate limit of a model of HIV replication and mutation, which we justify using methods from statistical physics. EMF outputs a set of time-dependent \"effective fitnesses\" that crucially depend on epistatic interactions and the sequence background, as well as predictions of the frequencies of mutation at each HIV residue over time. As a proof of principle, we apply this method to the dynamics of the p24 gag protein infecting a host whose T cell responses are known. Specifically, we show how fitness costs and epistatic interactions in the fitness landscape, the relative strengths of T cell responses, and the HIV sequence background, impact the locations and time course of HIV escape mutations, consistent with previous work. We also describe features of longer-term dynamics, specifically reversions, in terms of the effective fitnesses yielded by EMF, and quantify the mean fitness and entropy of the intra-host population over time. Finally, we develop a stochastic population dynamics version of EMF, extending prior stochastic approaches to a time-varying population size that crucially depends on the fitness of strains existing in the intra-host population at each time. The EMF approach offers a framework for understanding features of HIV dynamics in terms of effective fitnesses, and allows for a more detailed study of how the fitness landscape and sequence background impact both the evolutionary and population dynamics of HIV, in a computationally tractable way.\n\nAuthor summaryAs fitness landscapes of HIV proteins become more accurately known, it may become possible to more faithfully predict the locations and timescales of HIV mutations arising in a host with known immune responses, which may inform the design of vaccine immunogens. However, existing approaches for computing HIV dynamics given a fitness landscape are limited to fixed-population-size stochastic simulations. Here, we present an alternative approach that we designate the evolutionary mean-field (EMF) method. It takes as input an HIV fitness landscape and the locations and strengths of host immune responses, and outputs a set of time-dependent \"effective fitnesses\" and frequencies of mutation at each HIV residue over time. EMF is the high-recombination-rate limit of a model of HIV replication and mutation, which we derive using methods from statistical physics. We apply EMF on an example to show how fitness costs and epistatic interactions in the fitness landscape, the relative strengths of host immune responses, and the HIV sequence background, impact the locations and time course of HIV mutations. We also develop a stochastic population dynamics version of EMF where population size changes crucially depend on the fitness of strains existing in the population at each time. EMF makes quick predictions of the dynamics of HIV mutations through the effective fitnesses, crucially taking into account the fitness landscape and sequence background, and enables more detailed studies of how these affect the evolutionary and population dynamics of HIV, in a computationally tractable way.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Chen, H., Kardar, M.. 2019-01-11. Mean-field computational approach to HIV dynamics on a fitness landscape. https://doi.org/10.1101/518704

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Geometry of antigenic evolution improves influenza vaccine selection

Anticipating antigenic evolution is essential for selecting effective seasonal influenza A/H3N2 vaccine strains. To this end, we integrated hemagglutination-inhibition and neutralization titers spanning 2002 to 2025 into a unified Bayesian antigenic map. The map resolves twelve antigenic clusters advancing in discrete steps, with several clusters co-circulating in most seasons. In 15 of 21 seasons, the WHO-recommended vaccine belonged to an earlier cluster than the dominant circulating cluster. The direction of each vaccine update relative to recent viral drift predicted vaccine effectiveness one season ahead in out-of-sample forecasts. Antigenic distance, the conventional measure of vaccine-virus match, was weakly associated with effectiveness until update direction was accounted for. Retrospectively ranking candidate strains by predicted effectiveness would have selected a strain predicted to outperform the WHO recommendation in every season, raising mean predicted effectiveness by 10 percentage points.

evolutionary biology

Evolutionary replay of duplicate-gene retention across independent whole-genome duplications

Whole-genome duplications repeatedly expose ancestral gene lineages to the same broad evolutionary outcome-retention or loss of duplicated copies-but it remains unclear whether this history replays similarly across evolutionary scales. We placed duplicate retention in shared hierarchical orthologous-group coordinates and compared percentile ranks defined within each event-wide mapped universe. Three independent angiosperm whole-genome duplications showed reproducible replay (global rank effect T-replay = 0.210, bootstrap 95% confidence interval 0.172-0.248; permutation P = 1/100,001). A plant reference-panel score specified before target outcomes were examined predicted retention after the Apple/Pear duplication ({rho} = 0.169, n = 373). Deep transfer was heterogeneous: the teleost-genome-duplication estimate was positive but unresolved ({rho} = 0.107, n = 151, 95% confidence interval -0.050 to 0.260), whereas transfer to the ancient budding-yeast whole-genome duplication (yeast WGD) was supported ({rho} = 0.280, n = 186). Independently reconstructed animal outcomes also replayed between teleost and Stylommatophora duplications (r = 0.226, n = 146, P = 0.00326), although the effect remained below a prespecified strong-effect threshold. A strict plant-animal comparison was limited to 25 deeply one-to-one lineages and was unresolved (r = 0.033, 95% confidence interval -0.303 to 0.340). Thus, ancestral gene-lineage identity contributes reproducibly to duplicate retention after independent whole-genome duplications, but replay is structured by evolutionary lineage and modified by event-specific history rather than governed by one universal gene-fate ranking.

evolutionary biology

A Hymenoptera-restricted gene mediating ant castes co-opts deeply conserved machinery to control organ size

Lineage-specific genes are widespread and have been implicated as phenotypic innovation inducers, but how they acquire complex developmental functions remains poorly understood. Ant queens and workers develop dramatically different organ sizes from identical genomes under juvenile hormone (JH) control, yet the molecular effectors translating JH signalling into caste-specific organ growth remain unknown. Here we identify torch, a Hymenoptera-restricted gene, as the most consistently gyne-biased and JH-responsive gene across 68 ant species. Knockdown of torch in virgin queens of Monomorium pharaonis produces a worker-like, multi-organ growth-restricted phenotype. Mechanistically, torch harbours an E-box-like motif activated by the JH receptor Gce-Tai and acts as a GA-repeat-binding transcription factor that regulates Hippo signalling, the deeply conserved organ-size control pathway in animals. Expressing torch heterologously in mice and a growth-restricted Drosophila background shows that the gene retained its general growth-promoting activity across more than 700 million years of animal evolution in lineages that lack the gene, establishing that its function is mediated through conserved rather than ant-specific machinery. A lineage-specific gene can therefore acquire complex morphogenetic function by co-opting ancient organ-size circuitry, providing a general route by which novel genes can drive phenotypic innovation.

evolutionary biology