Evidence map›Paper›PMID 21874023›Full record

ArticleNature immunology2011

The antiviral factor APOBEC3G enhances the recognition of HIV-infected primary T cells by natural killer cells.

Jason M Norman, Michael Mashiba, Lucy A McNamara, Adewunmi Onafuwa-Nuga, Estelle Chiari-Fort, Wenwen Shen, Kathleen L Collins

Abstract read
In one paragraph

Article in Nature immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Natural killer cells in antiviral immunity.Nature reviews. Immunology · 2022
    Review
  12. Article
  13. The frequency of defective genes inJournal of ginseng research · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Jason M NormanDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Michael Mashiba
Lucy A McNamara
Adewunmi Onafuwa-Nuga
Estelle Chiari-Fort
Wenwen Shen
Kathleen L Collins
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TODD, ROBERT F · 2001 to 2010
$5.9M
Molecular Mechanisms of HIV Disease PathogenesisR01AI051192 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 2003 to 2011
$3.4M
Molecular Mechanisms of HIV Disease PathogenesisR56AI051192 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 2006 to 2013
$738k
NCI NIH HHS P30 CA046592NCRR NIH HHS UL1 RR024986NCRR NIH HHS UL1RR024986NIAID NIH HHS R01 AI051192NIAID NIH HHS R56 AI051192NIAID NIH HHS T32 AI007413NIAID NIH HHS T32AI007413NIAMS NIH HHS P30 AR048310NIAMS NIH HHS P30AR048310NIGMS NIH HHS T32 GM007863NIGMS NIH HHS T32GM007863PHS HHS P30CAO46592
6 · The paper itself

Abstract

APOBEC3G (A3G) is an intrinsic antiviral factor that inhibits the replication of human immunodeficiency virus (HIV) by deaminating cytidine residues to uridine. This causes guanosine-to-adenosine hypermutation in the opposite strand and results in inactivation of the virus. HIV counteracts A3G through the activity of viral infectivity factor (Vif), which promotes degradation of A3G. We report that viral protein R (Vpr), which interacts with a uracil glycosylase, also counteracted A3G by diminishing the incorporation of uridine. However, this process resulted in activation of the DNA-damage-response pathway and the expression of natural killer (NK) cell-activating ligands. Our results show that pathogen-induced deamination of cytidine and the DNA-damage response to virus-mediated repair of the incorporation of uridine enhance the recognition of HIV-infected cells by NK cells.

Indexed as

APOBEC-3G DeaminaseCells, CulturedCytidine DeaminaseCytotoxicity, ImmunologicDNA DamageGene Products, vprHIVHumansKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily KT-LymphocytesUridineAPOBEC-3G DeaminaseAPOBEC3G protein, humanCytidine DeaminaseGene Products, vprKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily KUridine

Identifiers

PMID21874023
PMCPMC3530928
OpenAlexW2122989279

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.