Evidence map›Paper›PMID 24562630›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2014

Δ(9)-Tetrahydrocannabinol treatment during human monocyte differentiation reduces macrophage susceptibility to HIV-1 infection.

Julie C Williams, Sofia Appelberg, Bruce A Goldberger, Thomas W Klein, John W Sleasman, Maureen M Goodenow

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.2field-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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  12. Expression and Functions of the CBFrontiers in pharmacology · 2022
    Article
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  17. Targeting Cannabinoid Receptor 2 on Peripheral Leukocytes to Attenuate Inflammatory Mechanisms Implicated in HIV-Associated Neurocognitive Disorder.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  18. Review
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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

6 authors at 3 institutions in 1 country.

Julie C WilliamsDepartment of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, 2033 Mowry Road, Campus Box 103633, Gainesville, FL, 32610-3663, USA.
Sofia Appelberg
Bruce A Goldberger
Thomas W Klein
John W Sleasman
Maureen M Goodenow
University of Florida · USDuke University · USUniversity of South Florida · US

Funding

Adol. Medicine Trials Network for HIV/AIDS InterventionsU01HD040474 · NICHD · WESTAT, INC. · PI HARRIS, DONALD ROBERT · 2001 to 2016
$114.4M
LEADERSHIP GROUP FOR ADOLESCENT MEDICINE TRIALS NETWORKU01HD040533 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WILSON, CRAIG M · 2001 to 2016
$76.4M
Substance Use and Immunity in HIV+ Adolescents by Systems BiologyR01DA031017 · NIDA · UNIVERSITY OF FLORIDA · PI YIN, LI · 2010 to 2014
$4.4M
NICHD NIH HHS HD40474NICHD NIH HHS HD40533NICHD NIH HHS U01 HD040474NICHD NIH HHS U01 HD040533NIDA NIH HHS DA031017NIDA NIH HHS R01 DA031017
6 · The paper itself

Abstract

The major psychoactive component of marijuana, Δ(9)-tetrahydrocannabinol (THC), also acts to suppress inflammatory responses. Receptors for THC, CB1, CB2, and GPR55, are differentially expressed on multiple cell types including monocytes and macrophages, which are important modulators of inflammation in vivo and target cells for HIV-1 infection. Use of recreational and medicinal marijuana is increasing, but the consequences of marijuana exposure on HIV-1 infection are unclear. Ex vivo studies were designed to investigate effects on HIV-1 infection in macrophages exposed to THC during or following differentiation. THC treatment of primary human monocytes during differentiation reduced HIV-1 infection of subsequent macrophages by replication competent or single cycle CCR5 using viruses. In contrast, treatment of macrophages with THC immediately prior to or continuously following HIV-1 exposure failed to alter infection. Specific receptor agonists indicated that the THC effect during monocyte differentiation was mediated primarily through CB2. THC reduced the number of p24 positive cells with little to no effect on virus production per infected cell, while quantitation of intracellular viral gag pinpointed the THC effect to an early event in the viral life cycle. Cells treated during differentiation with THC displayed reduced expression of CD14, CD16, and CD163 and donor dependent increases in mRNA expression of selected viral restriction factors, suggesting a fundamental alteration in phenotype. Ultimately, the mechanism of THC suppression of HIV-1 infection was traced to a reduction in cell surface HIV receptor (CD4, CCR5 and CXCR4) expression that diminished entry efficiency.

Indexed as

Cell DifferentiationCells, CulturedDisease SusceptibilityDronabinolHIV-1HIV InfectionsHumansMacrophagesMonocytesDronabinol

Identifiers

PMID24562630
PMCPMC4019698
OpenAlexW2074076338

What OpenQuestion holds

Textmetadata
LicenceTDM
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.