Evidence map›Paper›PMID 21814282›Full record

ArticleNature2011

HIV-1 adaptation to NK-cell-mediated immune pressure.

Galit Alter, David Heckerman, Arne Schneidewind, Lena Fadda, Carl M Kadie, Jonathan M Carlson, Cesar Oniangue-Ndza, Maureen Martin, Bin Li, Salim I Khakoo and 3 more

Abstract read
In one paragraph

Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers.

0numbers the graph read from it
0cells of the map it votes in
237citing papers in PubMed
15.3field-weighted citation impact, top 1% 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

237 citing papers in PubMed, 338 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. NK-like and networked CD8bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. CXCR6Frontiers in immunology · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  20. Article

177 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

13 authors at 5 institutions in 2 countries.

Galit AlterRagon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129, USA.
David Heckerman
Arne Schneidewind
Lena Fadda
Carl M Kadie
Jonathan M Carlson
Cesar Oniangue-Ndza
Maureen Martin
Bin Li
Salim I Khakoo
Mary Carrington
Todd M Allen
Marcus Altfeld
Harvard University · USMicrosoft (United States) · USRagon Institute of MGH, MIT and Harvard · USScience Applications International Corporation (United States) · USImperial College London · GB

Funding

The impact of HIV viral diversity and cellular immunity on HIV pathogenesisP30AI060354 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI Daniel Lingwood · 2004 to 2026
$94.4M
Effects of genetic polymorphism in MHC, KIR, and related loci on human diseaseZIABC010791 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CARRINGTON, MARY N. · 2009 to 2025
$18.2M
Recognition of HIV-1 by Innate Immunity Receptors during Primary InfectionP01AI074415 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALLEN, TODD M · 2008 to 2013
$17.3M
NK cell mediated immune pressure in HIV-1 infectionR01AI067031 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALTFELD, MARCUS · 2006 to 2015
$4.4M
CCR NIH HHS HHSN261200800001CIntramural NIH HHSNCI NIH HHS HHSN261200800001ENIAID NIH HHS P01 AI074415NIAID NIH HHS P30 AI060354NIAID NIH HHS R01 AI067031Wellcome Trust
6 · The paper itself

Abstract

Natural killer (NK) cells have an important role in the control of viral infections, recognizing virally infected cells through a variety of activating and inhibitory receptors. Epidemiological and functional studies have recently suggested that NK cells can also contribute to the control of HIV-1 infection through recognition of virally infected cells by both activating and inhibitory killer immunoglobulin-like receptors (KIRs). However, it remains unknown whether NK cells can directly mediate antiviral immune pressure in vivo in humans. Here we describe KIR-associated amino-acid polymorphisms in the HIV-1 sequence of chronically infected individuals, on a population level. We show that these KIR-associated HIV-1 sequence polymorphisms can enhance the binding of inhibitory KIRs to HIV-1-infected CD4(+) T cells, and reduce the antiviral activity of KIR-positive NK cells. These data demonstrate that KIR-positive NK cells can place immunological pressure on HIV-1, and that the virus can evade such NK-cell-mediated immune pressure by selecting for sequence polymorphisms, as was previously described for virus-specific T cells and neutralizing antibodies. NK cells might therefore have a previously underappreciated role in contributing to viral evolution.

Indexed as

Evolution, MolecularAdaptation, PhysiologicalAntibodies, NeutralizingCD4-Positive T-LymphocytesDecision Treesenv Gene Products, Human Immunodeficiency VirusGenotypeHIV-1HIV InfectionsHost-Pathogen InteractionsHuman Immunodeficiency Virus ProteinsHumansImmune EvasionKiller Cells, NaturalPolymorphism, GeneticReceptors, KIRAntibodies, Neutralizingenv Gene Products, Human Immunodeficiency VirusHuman Immunodeficiency Virus ProteinsKIR2DL2 protein, humanReceptors, KIRReceptors, KIR2DL2Viral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1

Identifiers

PMID21814282
PMCPMC3194000
OpenAlexW1993071851

What OpenQuestion holds

Textmetadata
LicenceTDM
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.