Evidence map›Paper›PMID 10644342›Full record

ArticleJournal of virology2000

Multiple integrations of human foamy virus in persistently infected human erythroleukemia cells.

C D Meiering, K E Comstock, M L Linial

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Nonintegrating foamy virus vectors.Journal of virology · 2010
    Article
  5. Viruses and thyroiditis: an update.Virology journal · 2009
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Foamy virus integration.Journal of virology · 2004
    Article
  12. Article
  13. Article
  14. Reactivation of a complex retrovirus is controlled by a molecular switch and is inhibited by a viral protein.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  15. Article
  16. Article
  17. Article
  18. Article
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

3 authors at 2 institutions in 1 country.

C D MeieringDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
K E Comstock
M L Linial
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

TRAINING IN MOLECULAR AND CELLULAR BIOLOGYT32GM007270 · NIGMS · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2020
$21.0M
Interdisciplinary Tranining in Cancer ResearchT32CA080416 · NCI · UNIVERSITY OF WASHINGTON · PI STODDARD, BARRY L. · 1998 to 2023
$9.7M
TARGETING RETROVIRAL VECTORS TO HEMATOPOIETIC STEM CELLSP01HL053762 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI KAN, YUET W · 1994 to 2004
$5.1M
VIRAL CODED FUNCTIONS IN ROUS SARCOMA VIRUSR01CA018282 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LINIAL, MAXINE L · 1985 to 2011
$5.0M
VIRAL ONCOLOGYT32CA009229 · NCI · UNIVERSITY OF WASHINGTON · PI LINIAL, MAXINE L · 1985 to 2007
$3.0M
NCI NIH HHS R01 CA018282NCI NIH HHS R01 CA18282NCI NIH HHS T32 CA009229NCI NIH HHS T32 CA080416NHLBI NIH HHS P01 HL053762NHLBI NIH HHS P01 HL53762NIGMS NIH HHS T32 GM007270NIGMS NIH HHS T32 GM07270
6 · The paper itself

Abstract

Foamy viruses are complex retroviruses whose replication strategy resembles that of conventional retroviruses. However, foamy virus replication also resembles that of hepadnaviruses in many respects. Because hepadnaviruses replicate in an integrase-independent manner, we were interested in investigating the characteristics of human foamy virus (HFV) integration. We have shown that HFV requires a functional integrase protein for infectivity. Our analyses have revealed that in single-cell clones derived from HFV-infected erythroleukemia-derived cells (H92), there were up to 20 proviral copies per host cell genome as determined by Southern blot and fluorescent in situ hybridization analysis. Use of specific probes has also shown that a majority of the proviruses contain the complete tas gene, which encodes the viral transactivator, and are not derived from Deltatas cDNAs, which have been shown to arise rapidly in infected cells. To demonstrate that the multiple proviral sequences are due to integration instead of recombination, we have sequenced the junctions between the proviral sequences and the host genome and found that the proviruses have authentic long terminal repeat ends and that each integration is at a different chromosomal site. A virus lacking the Gag nuclear localization signal accumulates fewer proviruses, suggesting that nuclear translocation is important for high proviral load. Since persistently infected H92 clones are not resistant to superinfection, the relative importance of an intracellular versus extracellular mechanism in proviral acquisition has yet to be determined.

Indexed as

Virus IntegrationVirus LatencyAnimalsBase SequenceCell LineCricetinaeDNA, ViralGene Products, gagHumansIntegrasesLeukemia, Erythroblastic, AcuteMolecular Sequence DataProvirusesSpumavirusTumor Cells, CulturedDNA, ViralGene Products, gagIntegrases

Identifiers

PMID10644342
PMCPMC111647
OpenAlexW2097735738

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.