Evidence map›Paper›PMID 27639573›Full record

ArticleVirology2016

Porphyromonas gingivalis-mediated signaling through TLR4 mediates persistent HIV infection of primary macrophages.

Luis M Agosto, Juliane B Hirnet, Daniel H Michaels, Yazdani B Shaik-Dasthagirisaheb, Frank C Gibson, Gregory Viglianti, Andrew J Henderson

Open access · hybridAbstract read
In one paragraph

Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. A functional screen identifies transcriptional networks that regulate HIV-1 and HIV-2.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  3. Article
  4. Article
  5. Article
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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

7 authors at 3 institutions in 1 country.

Luis M AgostoDepartment of Medicine, Section of Infectious Diseases, Boston Medical Center, Boston, MA, USA. Electronic address: agosto@bu.edu.
Juliane B HirnetDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA.
Daniel H MichaelsDepartment of Medicine, Section of Infectious Diseases, Boston Medical Center, Boston, MA, USA.
Yazdani B Shaik-DasthagirisahebDepartment of Medicine, Section of Infectious Diseases, Boston Medical Center, Boston, MA, USA.
Frank C GibsonDepartment of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL 32610-0424, USA.
Gregory VigliantiDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA.
Andrew J HendersonDepartment of Medicine, Section of Infectious Diseases, Boston Medical Center, Boston, MA, USA; Department of Microbiology, Boston University School of Medicine, Boston, MA, USA. Electronic address: andrew.henderson@bmc.org.
Boston Medical Center · USBoston University · USUniversity of Florida · US

Funding

Translational ScienceP30AI042853 · NIAID · MIRIAM HOSPITAL · PI LARRY K BROWN · 1998 to 2026
$51.7M
Transcription mechanisms that contribute to HIV-1 latencyR01AI097117 · NIAID · BOSTON MEDICAL CENTER · PI HENDERSON, ANDREW J · 2013 to 2016
$1.7M
Oral Macrophage Function in the Context of Periodontal Disease and HIV InfectionR56DE023950 · NIDCR · BOSTON MEDICAL CENTER · PI GIBSON, FRANK C, HENDERSON, ANDREW J · 2013 to 2014
$1.1M
Identification of Signals Required for the Establishment of HIV Infection and LatencyR56AI118682 · NIAID · BOSTON MEDICAL CENTER · PI HENDERSON, ANDREW J · 2015 to 2015
$761k
Novel compounds that target HIV latencyR21AI108447 · NIAID · BOSTON MEDICAL CENTER · PI HENDERSON, ANDREW J · 2014 to 2015
$488k
Transcriptional mechanisms that contribute to HIV-1 latencyR56AI097117 · NIAID · BOSTON MEDICAL CENTER · PI HENDERSON, ANDREW J · 2011 to 2011
$433k
NIAID NIH HHS P30 AI042853NIAID NIH HHS R01 AI097117NIAID NIH HHS R21 AI108447NIAID NIH HHS R56 AI097117NIAID NIH HHS R56 AI118682NIDCR NIH HHS R56 DE023950
6 · The paper itself

Abstract

Periodontal infections contribute to HIV-associated co-morbidities in the oral cavity and provide a model to interrogate the dysregulation of macrophage function, inflammatory disease progression, and HIV replication during co-infections. We investigated the effect of Porphyromonas gingivalis on the establishment of HIV infection in monocyte-derived macrophages. HIV replication in macrophages was significantly repressed in the presence of P. gingivalis. This diminished viral replication was due partly to a decrease in the expression of integrated HIV provirus. HIV repression depended upon signaling through TLR4 as knock-down of TLR4 with siRNA rescued HIV expression. Importantly, HIV expression was reactivated upon removal of P. gingivalis. Our observations suggest that exposure of macrophages to Gram-negative bacteria influence the establishment and maintenance of HIV persistence in macrophages through a TLR4-dependent mechanism.

Indexed as

Microbial InteractionsSignal TransductionAntigens, SurfaceGene Expression Regulation, ViralGene Knockdown TechniquesHIV-1HIV InfectionsHumansImmunophenotypingLeukocytes, MononuclearMacrophagesPhenotypePorphyromonas gingivalisToll-Like Receptor 4Virus ReplicationAntigens, SurfaceToll-Like Receptor 4

Identifiers

PMID27639573
PMCPMC5126732
OpenAlexW2518929177

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.