Evidence map›Paper›PMID 26366056›Full record

ArticleDrug design, development and therapy2015

Inhibition of HIV-1 by curcumin A, a novel curcumin analog.

Namita Kumari, Amol A Kulkarni, Xionghao Lin, Charlee McLean, Tatiana Ammosova, Andrey Ivanov, Maria Hipolito, Sergei Nekhai, Evaristus Nwulia

Open access · goldAbstract readComparative Study
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  5. Envelope Protein-Targeting Zika Virus Entry Inhibitors.International journal of molecular sciences · 2024
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  19. Article
  20. 2D layered nanomaterials for therapeutics delivery.Current opinion in biomedical engineering · 2021
    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

9 authors at 2 institutions in 2 countries.

Namita KumariTranslational Neuroscience Laboratory, Howard University, Washington, DC, USA ; Department of Medicine, Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC, USA.
Amol A KulkarniCollege of Pharmacy, Howard University, Washington, DC, USA.
Xionghao LinDepartment of Medicine, Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC, USA.
Charlee McLeanTranslational Neuroscience Laboratory, Howard University, Washington, DC, USA.
Tatiana AmmosovaDepartment of Medicine, Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC, USA.
Andrey IvanovDepartment of Medicine, Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC, USA.
Maria HipolitoTranslational Neuroscience Laboratory, Howard University, Washington, DC, USA.
Sergei NekhaiDepartment of Medicine, Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC, USA.
Evaristus NwuliaTranslational Neuroscience Laboratory, Howard University, Washington, DC, USA.
Translational Research in Oncology · FRHoward University · US

Funding

Therapeutics Targeting Filoviral interferon-antagonist and replication functionsU19AI109664 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BASLER, CHRISTOPHER F · 2014 to 2018
$15.8M
PROTEOMICS CORE FACILITYG12MD007597 · NIMHD · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 2012 to 2018
$14.8M
The District of Columbia Developmental Center for AIDS Research (DC D-CFAR)P30AI087714 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI GREENBERG, ALAN EDWARD · 2010 to 2014
$8.4M
Center for Hemoglobin Research in Minorities (CHaRM)P50HL118006 · NHLBI · HOWARD UNIVERSITY · PI NEKHAI, SERGEI · 2013 to 2017
$7.0M
Sickle Cell Disease and Sickle Cell Trait Protection Against HIV-1-infection in Africans and African AmericansR01HL125005 · NHLBI · HOWARD UNIVERSITY · PI MARINA A JEREBTSOVA, SERGEI NEKHAI · 2014 to 2026
$6.7M
Mediators of Lithium Action in Olfactory EpitheliumR01MH091460 · NIMH · HOWARD UNIVERSITY · PI NWULIA, EVARISTUS A · 2011 to 2015
$2.8M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENHLBI NIH HHS 1P50HL118006NHLBI NIH HHS 1R01HL125005NHLBI NIH HHS P50 HL118006NHLBI NIH HHS R01 HL125005NIAID NIH HHS P30 AI087714NIAID NIH HHS P30AI087714NIAID NIH HHS U19 AI109664NIAID NIH HHS U19AI109664NIMHD NIH HHS 5G12MD007597NIMHD NIH HHS G12 MD007597NIMH NIH HHS 5R01MH091460-03NIMH NIH HHS R01 MH091460
6 · The paper itself

Abstract

Despite the remarkable success of combination antiretroviral therapy at curtailing HIV progression, emergence of drug-resistant viruses, chronic low-grade inflammation, and adverse effects of combination antiretroviral therapy treatments, including metabolic disorders collectively present the impetus for development of newer and safer antiretroviral drugs. Curcumin, a phytochemical compound, was previously reported to have some in vitro anti-HIV and anti-inflammatory activities, but poor bioavailability has limited its clinical utility. To circumvent the bioavailability problem, we derivatized curcumin to sustain retro-aldol decomposition at physiological pH. The lead compound derived, curcumin A, showed increased stability, especially in murine serum where it was stable for up to 25 hours, as compared to curcumin that only had a half-life of 10 hours. Both curcumin and curcumin A showed similar inhibition of one round of HIV-1 infection in cultured lymphoblastoid (also called CEM) T cells (IC50=0.7 μM). But in primary peripheral blood mononuclear cells, curcumin A inhibited HIV-1 more potently (IC50=2 μM) compared to curcumin (IC50=12 μM). Analysis of specific steps of HIV-1 replication showed that curcumin A inhibited HIV-1 reverse transcription, but had no effect on HIV-1 long terminal repeat basal or Tat-induced transcription, or NF-κB-driven transcription at low concentrations that affected reverse transcription. Finally, we showed curcumin A induced expression of HO-1 and decreased cell cycle progression of T cells. Our findings thus indicate that altering the core structure of curcumin could yield more stable compounds with potent antiretroviral and anti-inflammatory activities.

Indexed as

AnimalsAnti-HIV AgentsCell Cycle CheckpointsCells, CulturedCurcuminDose-Response Relationship, DrugDrug StabilityEnzyme InductionGene Expression Regulation, ViralHalf-LifeHeme Oxygenase-1HIV-1HIV Reverse TranscriptaseHumansMiceReverse Transcriptase InhibitorsAnti-HIV AgentsCurcuminHeme Oxygenase-1HIV Reverse TranscriptaseHMOX1 protein, humanreverse transcriptase, Human immunodeficiency virus 1Reverse Transcriptase Inhibitorscurcumin Aheme oxygenase-1HIV-1reverse transcription

Identifiers

PMID26366056
PMCPMC4562762
OpenAlexW2150834336

What OpenQuestion holds

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LicenceCC BY-NC
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.