Evidence map›Paper›PMID 27363520›Full record

ArticleScientific reports2016

Inhibition of HIV-1 reactivation by a telomerase-derived peptide in a HSP90-dependent manner.

Hong Kim, Myung-Soo Choi, Kyung-Soo Inn, Bum-Joon Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
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  7. HIV Reservoirs and Treatment Strategies toward Curing HIV Infection.International journal of molecular sciences · 2024
    Review
  8. Review
  9. The heat shock response and small molecule regulators.European journal of medicinal chemistry · 2021
    Review
  10. Review
  11. Article
  12. Review
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  14. Article
  15. Review
  16. Article
  17. Telomerase-Targeted Cancer Immunotherapy.International journal of molecular sciences · 2019
    Review
  18. Article
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  20. 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

4 authors at 2 institutions in 1 country.

Hong KimDepartment of Microbiology and Immunology, Liver Research Institute, Biomedical Sciences and SNUMRC, College of Medicine, Seoul National University, Seoul, Korea.
Myung-Soo ChoiDepartment of Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul, Korea.
Kyung-Soo InnDepartment of Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul, Korea.
Bum-Joon KimDepartment of Microbiology and Immunology, Liver Research Institute, Biomedical Sciences and SNUMRC, College of Medicine, Seoul National University, Seoul, Korea.
Kyung Hee University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A peptide vaccine designed to induce T-cell immunity to telomerase, GV1001, has been shown to modulate cellular signaling pathways and confer a direct anti-cancer effect through the interaction with heat shock protein (HSP) 90 and 70. Here, we have found that GV1001 can modulate transactivation protein-mediated human immunodeficiency virus (HIV)-1 transactivation in an HSP90-dependent manner. GV1001 treatment resulted in significant suppression of HIV-1 replication and rescue of infected cells from death by HIV-1. Transactivation of HIV-long terminal repeat (LTR) was inhibited by GV1001, indicating that GV1001 suppressed the transcription from proviral HIV DNA. The anti-HIV-1 activity of GV1001 was completely abrogated by an HSP90-neutralizing antibody, indicating that the antiviral activity depends on HSP90. Further mechanistic studies revealed that GV1001 suppresses basal NF-κB activation, which is required for HIV-1 LTR transactivation in an HSP90-dependent manner. Inhibition of LTR transactivation by GV1001 suggests its potential to suppress HIV-1 reactivation from latency. Indeed, PMA-mediated reactivation of HIV-1 from latent infected cells was suppressed by GV1001. The results suggest the potential therapeutic use of GV1001, a peptide proven to be safe for human use, as an anti-HIV-1 agent to suppress the reactivation from latently infected cells.

Indexed as

Amino Acid SequenceCell Line, TumorCell SurvivalGene Expression Regulation, ViralHIV-1HSP90 Heat-Shock ProteinsHumansJurkat CellsNeoplasmsPeptide FragmentsProtein BindingTelomeraseVaccines, SubunitVirus ActivationVirus LatencyVirus ReplicationGV1001 peptideHSP90 Heat-Shock ProteinsPeptide FragmentsTelomeraseVaccines, Subunit

Identifiers

PMID27363520
PMCPMC4929463
OpenAlexW2471449754

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.