ArticlePLoS pathogens2014
The contribution of viral genotype to plasma viral set-point in HIV infection.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed.
- Circumcision status at HIV infection is not associated with plasma viral load in men: analysis of specimens from a randomized controlled trial.BMC infectious diseases · 2018Trial
- Detectable effects of bacterial phylogeny on virulence but not phage efficacy in anISME communications · 2026Article
- Attenuation of HIV severity by slightly deleterious mutations can explain the long-term trajectory of virulence evolution.PLoS computational biology · 2025Article
- The genetic architecture of HIV-1 virulence.Virus evolution · 2025Article
- Reconciling founder variant multiplicity of HIV-1 infection with the rate of CD4Journal of the Royal Society, Interface · 2024Article
- A Phylogeny-aware GWAS Framework to Correct for Heritable Pathogen Effects on Infectious Disease Traits.Molecular biology and evolution · 2022Article
- Inferring Phenotypic Trait Evolution on Large Trees With Many Incomplete Measurements.Journal of the American Statistical Association · 2022Article
- HIV-1 Entry and Prospects for Protecting against Infection.Microorganisms · 2021Review
- Heritability of the HIV-1 reservoir size and decay under long-term suppressive ART.Nature communications · 2020Article
- Proliferation and benevolence-A framework for dissecting the mechanisms of microbial virulence and health promotion.Evolutionary applications · 2020Article
- TheFuture virology · 2020Review
- Natural selection favoring more transmissible HIV detected in United States molecular transmission network.Nature communications · 2019Article
- Automatic generation of evolutionary hypotheses using mixed Gaussian phylogenetic models.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A Practical Guide to Estimating the Heritability of Pathogen Traits.Molecular biology and evolution · 2018Article
- Dissecting HIV Virulence: Heritability of Setpoint Viral Load, CD4+ T-Cell Decline, and Per-Parasite Pathogenicity.Molecular biology and evolution · 2018Article
- Interaction of the Host and Viral Genome and Their Influence on HIV Disease.Frontiers in genetics · 2018Review
- Viral genetic variation accounts for a third of variability in HIV-1 set-point viral load in Europe.PLoS biology · 2017Article
- Parent-offspring regression to estimate the heritability of an HIV-1 trait in a realistic setup.Retrovirology · 2017Article
- Estimating the Respective Contributions of Human and Viral Genetic Variation to HIV Control.PLoS computational biology · 2017Article
- Emerging Concepts of Data Integration in Pathogen Phylodynamics.Systematic biology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Disease progression in HIV-infected individuals varies greatly, and while the environmental and host factors influencing this variation have been widely investigated, the viral contribution to variation in set-point viral load, a predictor of disease progression, is less clear. Previous studies, using transmission-pairs and analysis of phylogenetic signal in small numbers of individuals, have produced a wide range of viral genetic effect estimates. Here we present a novel application of a population-scale method based in quantitative genetics to estimate the viral genetic effect on set-point viral load in the UK subtype B HIV-1 epidemic, based on a very large data set. Analyzing the initial viral load and associated pol sequence, both taken before anti-retroviral therapy, of 8,483 patients, we estimate the proportion of variance in viral load explained by viral genetic effects to be 5.7% (CI 2.8-8.6%). We also estimated the change in viral load over time due to selection on the virus and environmental effects to be a decline of 0.05 log10 copies/mL/year, in contrast to recent studies which suggested a reported small increase in viral load over the last 20 years might be due to evolutionary changes in the virus. Our results suggest that in the UK epidemic, subtype B has a small but significant viral genetic effect on viral load. By allowing the analysis of large sample sizes, we expect our approach to be applicable to the estimation of the genetic contribution to traits in many organisms.
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Registered trials
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.