Evidence map›Paper›PMID 21124991›Full record

ArticlePLoS pathogens2010

Modelling the evolution and spread of HIV immune escape mutants.

Helen R Fryer, John Frater, Anna Duda, Mick G Roberts, SPARTAC Trial Investigators, Rodney E Phillips, Angela R McLean

Open access · goldAbstract 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 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

43 citing papers in PubMed, 70 citations in OpenAlex.

  1. A binary trait model reveals the fitness effects of HIV-1 escape from T cell responses.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Compartmental structure in the secondary lymphoid tissue can slow downJournal of the Royal Society, Interface · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Evolution during primary HIV infection does not require adaptive immune selection.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Neutral Theory and Rapidly Evolving Viral Pathogens.Molecular biology and evolution · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

7 authors at 3 institutions in 2 countries.

Helen R FryerDepartment of Zoology, Oxford University, Oxford, UK.
John Frater
Anna Duda
Mick G Roberts
SPARTAC Trial Investigators
Rodney E Phillips
Angela R McLean
Medawar Building for Pathogen Research · GBUniversity of Oxford · GBMassey University · NZ

Funding

Medical Research Council G108/626Medical Research Council MC_U122886352Medical Research Council MC_U950097145Wellcome Trust
6 · The paper itself

Abstract

During infection with human immunodeficiency virus (HIV), immune pressure from cytotoxic T-lymphocytes (CTLs) selects for viral mutants that confer escape from CTL recognition. These escape variants can be transmitted between individuals where, depending upon their cost to viral fitness and the CTL responses made by the recipient, they may revert. The rates of within-host evolution and their concordant impact upon the rate of spread of escape mutants at the population level are uncertain. Here we present a mathematical model of within-host evolution of escape mutants, transmission of these variants between hosts and subsequent reversion in new hosts. The model is an extension of the well-known SI model of disease transmission and includes three further parameters that describe host immunogenetic heterogeneity and rates of within host viral evolution. We use the model to explain why some escape mutants appear to have stable prevalence whilst others are spreading through the population. Further, we use it to compare diverse datasets on CTL escape, highlighting where different sources agree or disagree on within-host evolutionary rates. The several dozen CTL epitopes we survey from HIV-1 gag, RT and nef reveal a relatively sedate rate of evolution with average rates of escape measured in years and reversion in decades. For many epitopes in HIV, occasional rapid within-host evolution is not reflected in fast evolution at the population level.

Indexed as

Biological EvolutionModels, TheoreticalEpitopes, T-Lymphocytegag Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsHIV Reverse TranscriptaseHumansMutationnef Gene Products, Human Immunodeficiency VirusPhylogenyT-Lymphocytes, CytotoxicEpitopes, T-Lymphocytegag Gene Products, Human Immunodeficiency VirusHIV Reverse Transcriptasenef Gene Products, Human Immunodeficiency Virusreverse transcriptase, Human immunodeficiency virus 1

Identifiers

PMID21124991
PMCPMC2987822
OpenAlexW2163591597

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.