Evidence map›Paper›PMID 20941398›Full record

ArticlePLoS pathogens2010

Phylogenetic approach reveals that virus genotype largely determines HIV set-point viral load.

Samuel Alizon, Viktor von Wyl, Tanja Stadler, Roger D Kouyos, Sabine Yerly, Bernard Hirschel, Jürg Böni, Cyril Shah, Thomas Klimkait, Hansjakob Furrer and 9 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  11. Different diets and their effect on tuberculosis prevention in HIV patients.Journal of family medicine and primary care · 2022
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  20. Automatic generation of evolutionary hypotheses using mixed Gaussian phylogenetic models.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article

20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Samuel AlizonInstitute of Integrative Biology, ETH Zürich, Zürich, Switzerland. samuel.alizon@montp.cnrs.fr
Viktor von Wyl
Tanja Stadler
Roger D Kouyos
Sabine Yerly
Bernard Hirschel
Jürg Böni
Cyril Shah
Thomas Klimkait
Hansjakob Furrer
Andri Rauch
Pietro L Vernazza
Enos Bernasconi
Manuel Battegay
Philippe Bürgisser
Amalio Telenti
Huldrych F Günthard
Sebastian Bonhoeffer
Swiss HIV Cohort Study

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV virulence, i.e. the time of progression to AIDS, varies greatly among patients. As for other rapidly evolving pathogens of humans, it is difficult to know if this variance is controlled by the genotype of the host or that of the virus because the transmission chain is usually unknown. We apply the phylogenetic comparative approach (PCA) to estimate the heritability of a trait from one infection to the next, which indicates the control of the virus genotype over this trait. The idea is to use viral RNA sequences obtained from patients infected by HIV-1 subtype B to build a phylogeny, which approximately reflects the transmission chain. Heritability is measured statistically as the propensity for patients close in the phylogeny to exhibit similar infection trait values. The approach reveals that up to half of the variance in set-point viral load, a trait associated with virulence, can be heritable. Our estimate is significant and robust to noise in the phylogeny. We also check for the consistency of our approach by showing that a trait related to drug resistance is almost entirely heritable. Finally, we show the importance of taking into account the transmission chain when estimating correlations between infection traits. The fact that HIV virulence is, at least partially, heritable from one infection to the next has clinical and epidemiological implications. The difference between earlier studies and ours comes from the quality of our dataset and from the power of the PCA, which can be applied to large datasets and accounts for within-host evolution. The PCA opens new perspectives for approaches linking clinical data and evolutionary biology because it can be extended to study other traits or other infectious diseases.

Indexed as

PhylogenyAnti-HIV AgentsGenotypeHIV-1HIV InfectionsHumansModels, StatisticalQuantitative Trait LociRNA, ViralViral LoadAnti-HIV AgentsRNA, Viral

Identifiers

PMID20941398
PMCPMC2947993

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Registered trials

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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.