Evidence map›Paper›PMID 15911774›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

The antiretroviral activity of APOBEC3 is inhibited by the foamy virus accessory Bet protein.

Martin Löchelt, Fabian Romen, Patrizia Bastone, Heide Muckenfuss, Nadine Kirchner, Yong-Boum Kim, Uwe Truyen, Uwe Rösler, Marion Battenberg, Ali Saib and 3 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
10.0field-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

123 citing papers in PubMed, 184 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. HIV-1 latency: From acquaintance to confidant.Journal of virus eradication · 2025
    Review
  6. Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Foamy Virus Integrase in Development of Viral Vector for Gene Therapy.Journal of microbiology and biotechnology · 2020
    Review
  19. Article
  20. Review

63 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 3 institutions in 1 country.

Martin LöcheltDepartment Genome Modifications and Carcinogenesis, Focus Infection and Cancer, German Cancer Research Center, 69009 Heidelberg, Germany.
Fabian Romen
Patrizia Bastone
Heide Muckenfuss
Nadine Kirchner
Yong-Boum Kim
Uwe Truyen
Uwe Rösler
Marion Battenberg
Ali Saib
Egbert Flory
Klaus Cichutek
Carsten Münk
German Cancer Research Center · DEPaul Ehrlich Institut · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome hypermutation of different orthoretroviruses by cellular cytidine deaminases of the APOBEC3 family during reverse transcription has recently been observed. Lentiviruses like HIV-1 have acquired proteins preventing genome editing in the newly infected cell. Here we show that feline foamy virus (FFV), a typical member of the foamy retrovirus subfamily Spumaretrovirinae, is also refractory to genome deamination. APOBEC3-like FFV genome editing in APOBEC3-positive feline CRFK cells only occurs when the accessory FFV Bet protein is functionally inactivated. Editing of bet-deficient FFV genomes is paralleled by a strong decrease in FFV titer. In contrast to lentiviruses, cytidine deamination already takes place in APOBEC3-positive FFV-producing cells, because edited proviral DNA genomes are consistently present in released particles. By cloning the feline APOBEC3 orthologue, we found that its homology to the second domain of human APOBEC3F is 48%. Expression of feline APOBEC3 in APOBEC3-negative human 293T cells reproduced the effects seen in homologous CRFK cells: Bet-deficient FFV displayed severely reduced titers, high-level genome editing, reduced particle release, and suppressed Gag processing. Although WT Bet efficiently preserved FFV infectivity and genome integrity, it sustained particle release and Gag processing only when fe3 was moderately expressed. Similar to lentiviral Vif proteins, FFV Bet specifically bound feline APOBEC3. In particles from Bet-deficient FFV, feline APOBEC3 was clearly present, whereas its foamy viral antagonist Bet was undetectable in purified WT particles. This is the first report that, in addition to lentiviruses, the foamy viruses also developed APOBEC3-counter-acting proteins.

Indexed as

GenomeAmino Acid SequenceAnimalsBlotting, WesternCatsCell LineCloning, MolecularCodonCytidine DeaminaseDNA, ComplementaryDNA PrimersHumansImmunoprecipitationMolecular Sequence DataMutationPlasmidsCodonCytidine DeaminaseDNA, ComplementaryDNA PrimersRetroviridae Proteins

Identifiers

PMID15911774
PMCPMC1142374
OpenAlexW2073978153

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.