Evidence map›Paper›PMID 10400800›Full record

ArticleJournal of virology1999

Interleukin-16 inhibits human immunodeficiency virus type 1 entry and replication in macrophages and in dendritic cells.

M J Truong, E C Darcissac, E Hermann, J Dewulf, A Capron, G M Bahr

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 42 citations in OpenAlex.

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  6. Innate and adaptive factors regulating human immunodeficiency virus type 1 genomic activation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
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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 2 institutions in 1 country.

M J TruongInstitut Pasteur de Lille, INSERM U167, 59019 Lille Cedex, France.
E C Darcissac
E Hermann
J Dewulf
A Capron
G M Bahr
Institut Pasteur de Lille · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recombinant interleukin-16 (rIL-16) has been found to inhibit human immunodeficiency virus type 1 (HIV-1) replication in acutely or endogenously infected CD4(+) T cells. However, the effect of rIL-16 on HIV-1 replication in antigen-presenting cells (APCs) is still unknown. We show here a potent HIV-suppressive activity of rIL-16 in acutely infected monocyte-derived macrophages and dendritic cells determined by the levels of viral RNA transcripts or of viral reverse transcriptase in culture supernatants. The observed effect was dependent on the presence of rIL-16 early after infection and could not be induced by a 24-h treatment of cells with the cytokine prior to infection. Using macrophage-tropic and dually tropic primary isolates, we also showed that the addition of rIL-16 to cell cultures only during the infection period was effective in blocking virus entry and reducing proviral DNA levels in APCs. However, the anti-HIV activity of rIL-16 could not be linked to the induction of virus-suppressive concentrations of beta-chemokines or to the inhibition of HIV-enhancing cytokines. These findings establish a critical role for rIL-16 in protecting APCs against HIV-1 infection and lend further support to its potential use in the treatment of HIV disease.

Indexed as

Chemokine CCL4CytokinesDendritic CellsDNA, ViralGene ExpressionHIV-1HumansInterleukin-16Macrophage Inflammatory ProteinsMacrophagesProvirusesRecombinant ProteinsRNA, MessengerRNA, ViralVirus ReplicationChemokine CCL4CytokinesDNA, ViralInterleukin-16Macrophage Inflammatory ProteinsRecombinant ProteinsRNA, MessengerRNA, Viral

Identifiers

PMID10400800
PMCPMC112787
OpenAlexW2137798042

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.