ArticleGenetics2013
Computational inference methods for selective sweeps arising in acute HIV infection.
Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Kinetics of HIV-Specific CTL Responses Plays a Minimal Role in Determining HIV Escape Dynamics.Frontiers in immunology · 2018Article
- Within-Epitope Interactions Can Bias CTL Escape Estimation in Early HIV Infection.Frontiers in immunology · 2017Article
- Investigating the Consequences of Interference between Multiple CD8+ T Cell Escape Mutations in Early HIV Infection.PLoS computational biology · 2016Article
- Broad CTL Response in Early HIV Infection Drives Multiple Concurrent CTL Escapes.PLoS computational biology · 2015Article
- Immuno-epidemiological modeling of HIV-1 predicts high heritability of the set-point virus load, while selection for CTL escape dominates virulence evolution.PLoS computational biology · 2014Article
- Reliable reconstruction of HIV-1 whole genome haplotypes reveals clonal interference and genetic hitchhiking among immune escape variants.Retrovirology · 2014Article
- The Effect of Interference on the CD8(+) T Cell Escape Rates in HIV.Frontiers in immunology · 2014Article
- Inferring HIV Escape Rates from Multi-Locus Genotype Data.Frontiers in immunology · 2013Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the first weeks of human immunodeficiency virus-1 (HIV-1) infection, cytotoxic T-lymphocytes (CTLs) select for multiple escape mutations in the infecting HIV population. In recent years, methods that use escape mutation data to estimate rates of HIV escape have been developed, thereby providing a quantitative framework for exploring HIV escape from CTL response. Current methods for escape-rate inference focus on a specific HIV mutant selected by a single CTL response. However, recent studies have shown that during the first weeks of infection, CTL responses occur at one to three epitopes and HIV escape occurs through complex mutation pathways. Consequently, HIV escape from CTL response forms a complex, selective sweep that is difficult to analyze. In this work, we develop a model of initial infection, based on the well-known standard model, that allows for a description of multi-epitope response and the complex mutation pathways of HIV escape. Under this model, we develop Bayesian and hypothesis-test inference methods that allow us to analyze and estimate HIV escape rates. The methods are applied to two HIV patient data sets, concretely demonstrating the utility of our approach.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.