Evidence map›Paper›PMID 12808465›Full record

ArticleNature2003

The cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNA.

Hui Zhang, Bin Yang, Roger J Pomerantz, Chune Zhang, Shyamala C Arunachalam, Ling Gao

Open access · greenAbstract read
In one paragraph

Article in Nature, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 599 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
599citing papers in PubMed, 1 pooled it
27.6field-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

599 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,046 citations in OpenAlex.

  1. Pooled it
  2. Broad activation of latent HIV-1 in vivo.Nature communications · 2016
    Trial
  3. Mechanisms of HIV-1 assembly, release and maturation.Nature reviews. Microbiology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Collapsing retroviruses for efficient delivery of viro-toxic cargoes.bioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Journal of virology · 2025
    Article
  15. Fitness Landscapes of APOBEC3G Antagonism by HIV-1 Vif proteins.bioRxiv : the preprint server for biology · 2025
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hui ZhangThe Dorrance H. Hamilton Laboratories, Center for Human Virology and Biodefense, Division of Infectious Diseases and Environmental Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. hui.zhang@mail.tju.edu
Bin Yang
Roger J Pomerantz
Chune Zhang
Shyamala C Arunachalam
Ling Gao
Thomas Jefferson University · US

Funding

Role of HIV-1 VIF in Assembly of the RT ComplexR01AI047720 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, HUI · 2001 to 2004
$1.1M
NIAID NIH HHS R01 AI047720
6 · The paper itself

Abstract

High mutation frequency during reverse transcription has a principal role in the genetic variation of primate lentiviral populations. It is the main driving force for the generation of drug resistance and the escape from immune surveillance. G to A hypermutation is one of the characteristics of primate lentiviruses, as well as other retroviruses, during replication in vivo and in cell culture. The molecular mechanisms of this process, however, remain to be clarified. Here, we demonstrate that CEM15 (also known as apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G; APOBEC3G), an endogenous inhibitor of human immunodeficiency virus type 1 (HIV-1) replication, is a cytidine deaminase and is able to induce G to A hypermutation in newly synthesized viral DNA. This effect can be counteracted by the HIV-1 virion infectivity factor (Vif). It seems that this viral DNA mutator is a viral defence mechanism in host cells that may induce either lethal hypermutation or instability of the incoming nascent viral reverse transcripts, which could account for the Vif-defective phenotype. Importantly, the accumulation of CEM15-mediated non-lethal hypermutation in the replicating viral genome could potently contribute to the genetic variation of primate lentiviral populations.

Indexed as

APOBEC-3G DeaminaseCell LineCytidine DeaminaseDNA, ViralGene Products, vifHIV-1HumansMutagenesisNucleoside DeaminasesPoint MutationProteinsRepressor ProteinsSerial PassageTranscription, Geneticvif Gene Products, Human Immunodeficiency VirusVirus ReplicationAPOBEC-3G DeaminaseAPOBEC3G protein, humanCytidine DeaminaseDNA, ViralGene Products, vifNucleoside DeaminasesProteinsRepressor Proteinsvif Gene Products, Human Immunodeficiency Virus

Identifiers

PMID12808465
PMCPMC1350966
OpenAlexW2023035407

What OpenQuestion holds

Textmetadata
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.