Evidence map›Paper›PMID 8709190›Full record

ArticleJournal of virology1996

The human immunodeficiency virus type 1 capsid p2 domain confers sensitivity to the cyclophilin-binding drug SDZ NIM 811.

T Dorfman, H G Göttlinger

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. SIV replication in human cells.Frontiers in microbiology · 2012
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Cyclophilin A is required for TRIM5{alpha}-mediated resistance to HIV-1 in Old World monkey cells.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  19. Article
  20. In defense of the cell: TRIM5alpha interception of mammalian retroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2004
    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

2 authors at 1 institution in 1 country.

T DorfmanDivision of Human Retrovirology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
H G Göttlinger
Dana-Farber Cancer Institute · US

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI A. Heather Eliassen · 1985 to 2026
$330.6M
DFCI-BIDMC-CH CENTER FOR AIDS RESEARCHP30AI028691 · NIAID · DANA-FARBER CANCER INSTITUTE · PI SODROSKI, JOSEPH G · 1989 to 2003
$6.2M
Molecular Biology of HIV-Gag ProteinsR37AI029873 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GOTTLINGER, HEINRICH · 2004 to 2013
$5.1M
MOLECULAR BIOLOGY OF HIV GAG PROTEINSR01AI029873 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GOTTLINGER, HEINRICH · 1990 to 2018
$3.7M
NCI NIH HHS CA06516NIAID NIH HHS AI28691NIAID NIH HHS AI29873
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) specifically incorporates the host cell peptidyl-prolyl isomerase cyclophilin A into virions via contacts with the capsid (CA) domain of the Gag polyprotein Pr55gag. The immunosuppressant drug cyclosporin A and the nonimmunosuppressive cyclosporin A analog SDZ NIM 811 bind to cyclophilin A and inhibit its incorporation into HIV-1 virions. Both drugs inhibit the virion association of cyclophilin A and the replication of HIV-1 with a similar dose dependence. In contrast, these compounds are inactive against other primate lentiviruses which do not incorporate cyclophilin A, such as simian immunodeficiency virus (SIV). To locate determinants which confer sensitivity to SDZ NIM 811, we generated chimeric proviruses between HIV-1 and SIVmac. A hybrid SIVmac which has the CA-p2 domain of the Gag polyprotein replaced by the corresponding domain from HIV-1 replicated in an established CD4+ cell line and in human but not macaque peripheral blood mononuclear cells. The transfer of the HIV-1 CA-p2 domain to SIVmac led to the efficient incorporation of cyclophilin A, and SDZ NIM 811 effectively inhibited both the virion association of cyclophilin A and the spread of the hybrid virus in infected cultures. We conclude that the HIV-1 CA-p2 domain contains determinants which confer the necessity to interact with cyclophilin A for efficient virus replication. Furthermore, our data show that the CA-p2 domain can play a crucial role in species tropism.

Indexed as

Genes, gagAmino Acid IsomerasesAnimalsAntiviral AgentsBase SequenceCapsidCarrier ProteinsCell LineChimeraCloning, MolecularCyclosporineEndodeoxyribonucleasesGene Products, gagHIV-1HumansLymphocytesAmino Acid IsomerasesAntiviral AgentsCarrier ProteinsCyclosporineEndodeoxyribonucleasesGene Products, gag(melle-4)cyclosporinOligodeoxyribonucleotidesp55 gag precursor protein, Human immunodeficiency virus 1Peptidylprolyl IsomeraseProtein PrecursorsRecombinant Fusion Proteins

Identifiers

PMID8709190
PMCPMC190588
OpenAlexW2158685964

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.