Evidence map›Paper›PMID 27212475›Full record

ArticleNature communications2016

Relative rate and location of intra-host HIV evolution to evade cellular immunity are predictable.

John P Barton, Nilu Goonetilleke, Thomas C Butler, Bruce D Walker, Andrew J McMichael, Arup K Chakraborty

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
9.9field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 147 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Direct estimation of genotype fitness from time series.bioRxiv : the preprint server for biology · 2026
    Article
  5. Exploring novel kinetics of automated HMicrobiology spectrum · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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
  13. Article
  14. Article
  15. Article
  16. Article
  17. Modelling HIV-1 control and remission.NPJ systems biology and applications · 2024
    Review
  18. Kinetic coevolutionary models predict the temporal emergence of HIV-1 resistance mutations under drug selection pressure.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Review

16 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

6 authors at 5 institutions in 2 countries.

John P BartonRagon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts 02139, USA.ORCID http://orcid.org/0000-0003-1467-421X
Nilu GoonetillekeDepartment of Microbiology, Immunology and Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Thomas C ButlerDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Bruce D WalkerRagon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts 02139, USA.
Andrew J McMichaelNuffield Department of Medicine, University of Oxford, Old Road Campus, Headington, Oxford OX3 7FZ, UK.
Arup K ChakrabortyRagon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts 02139, USA.
Ragon Institute of MGH, MIT and Harvard · USHoward Hughes Medical Institute · USMassachusetts Institute of Technology · USUniversity of North Carolina at Chapel Hill · USUniversity of Oxford · GB

Funding

Virus biology scientific research support componentUM1AI100645 · NIAID · DUKE UNIVERSITY · PI MCMICHAEL, ANDREW JAMES · 2012 to 2018
$204.7M
Support Component D/Vaccine Discovery, Concept to ClinicUM1AI100663 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI BAROUCH, DAN H. · 2012 to 2018
$131.5M
Medical Research Council MR/K012037/1NIAID NIH HHS UM1 AI100645NIAID NIH HHS UM1 AI100663
6 · The paper itself

Abstract

Human immunodeficiency virus (HIV) evolves within infected persons to escape being destroyed by the host immune system, thereby preventing effective immune control of infection. Here, we combine methods from evolutionary dynamics and statistical physics to simulate in vivo HIV sequence evolution, predicting the relative rate of escape and the location of escape mutations in response to T-cell-mediated immune pressure in a cohort of 17 persons with acute HIV infection. Predicted and clinically observed times to escape immune responses agree well, and we show that the mutational pathways to escape depend on the viral sequence background due to epistatic interactions. The ability to predict escape pathways and the duration over which control is maintained by specific immune responses open the door to rational design of immunotherapeutic strategies that might enable long-term control of HIV infection. Our approach enables intra-host evolution of a human pathogen to be predicted in a probabilistic framework.

Indexed as

Evolution, MolecularGenetic FitnessFemaleHIVHIV InfectionsHuman Immunodeficiency Virus ProteinsHumansImmunity, CellularMaleModels, GeneticPolyproteinsHuman Immunodeficiency Virus ProteinsPolyproteins

Identifiers

PMID27212475
PMCPMC4879252
OpenAlexW2402027820

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.