Evidence map›Paper›PMID 17715216›Full record

ArticleJournal of virology2007

Analysis of human cell heterokaryons demonstrates that target cell restriction of cyclosporine-resistant human immunodeficiency virus type 1 mutants is genetically dominant.

Chisu Song, Christopher Aiken

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
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  9. Article
  10. Dynamic allostery governs cyclophilin A-HIV capsid interplay.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  11. Review
  12. Review
  13. Article
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  16. Article
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  19. TRIM5 and the Regulation of HIV-1 Infectivity.Molecular biology international · 2012
    Article
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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

2 authors at 1 institution in 1 country.

Chisu SongDepartment of Microbiology and Immunology, Vanderbilt University School of Medicine, A-5301 Medical Center North, Nashville, TN 37232-2363, USA.
Christopher Aiken
Vanderbilt University Medical Center · US

Funding

Function of Viral Core Disassembly in HIV-1 InfectionR01AI050423 · NIAID · VANDERBILT UNIVERSITY · PI AIKEN, CHRISTOPHER R · 2002 to 2005
$1.1M
Mechanism of HIV-1 Restriction by TRIM5alphaR56AI050423 · NIAID · VANDERBILT UNIVERSITY · PI AIKEN, CHRISTOPHER R · 2006 to 2006
$306k
NIAID NIH HHS AI 050423NIAID NIH HHS R01 AI050423NIAID NIH HHS R56 AI050423
6 · The paper itself

Abstract

The host cell protein cyclophilin A (CypA) binds to CA of human immunodeficiency virus type 1 (HIV-1) and promotes HIV-1 infection of target cells. Disruption of the CypA-CA interaction, either by mutation of the CA residue at G89 or P90 or with the immunosuppressive drug cyclosporine (CsA), reduces HIV-1 infection. Two CA mutants, A92E and G94D, previously were identified by selection for growth of wild-type HIV-1 in cultures of CD4(+) HeLa cell cultures containing CsA. Interestingly, infection of some cell lines by these mutants is enhanced in the presence of CsA, while in other cell lines these mutants are minimally affected by the drug. Little is known about this cell-dependent phenotype of the A92E and G94D mutants, except that it is not dependent on expression of the host factor TRIM5alpha. Here, we show that infection by the A92E and G94D mutants is restricted at an early post-entry stage of the HIV-1 life cycle. Analysis of heterokaryons between CsA-dependent HeLa-P4 cells and CsA-independent 293T cells indicated that the CsA-dependent infection by A92E and G94D mutants is due to a dominant cellular restriction. We also show that addition of CsA to target cells inhibits infection by wild-type HIV-1 prior to reverse transcription. Collectively, these results support the existence of a cell-specific human cellular factor capable of restricting HIV-1 at an early post-entry step by a CypA-dependent mechanism.

Indexed as

MutationVirus ReplicationAnti-HIV AgentsCell NucleusCyclosporineCytoplasmDrug ResistanceFlow CytometryGenes, DominantHeLa CellsHIV-1HumansPlasmidsVirionAnti-HIV AgentsCyclosporine

Identifiers

PMID17715216
PMCPMC2168785
OpenAlexW2118687179

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.