Evidence map›Paper›PMID 24903666›Full record

ArticleThe Journal of infectious diseases2014

Antigen-presenting phagocytic cells ingest malaria parasites and increase HIV replication in a tumor necrosis factor α-dependent manner.

Marika Orlov, Florin Vaida, Kathryn Williamson, Qianqian Deng, David M Smith, Patrick E Duffy, Robert T Schooley

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Article
  7. 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

7 authors at 2 institutions in 1 country.

Marika OrlovUniversity of California-San Diego, La Jolla Seattle Biomedical Research Institute, Washington.
Florin VaidaUniversity of California-San Diego, La Jolla.
Kathryn WilliamsonSeattle Biomedical Research Institute, Washington.
Qianqian DengUniversity of California-San Diego, La Jolla.
David M SmithUniversity of California-San Diego, La Jolla.
Patrick E DuffySeattle Biomedical Research Institute, Washington National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland.
Robert T SchooleyUniversity of California-San Diego, La Jolla.
University of California, San Diego · USCenter for Infectious Disease Research · US

Funding

VirologyP30AI036214 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Maile Ann Young Karris · 1994 to 2026
$78.4M
STRUCTURAL NEUROIMAGING COREP30MH062512 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DAVID J MOORE · 2001 to 2026
$50.4M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007198 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C, INSEL, PAUL A · 1985 to 2024
$29.3M
Preventing Pregnancy Malaria: Maternal-Infant OutcomesU19AI065664 · NIAID · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI OLEINIKOV, ANDREW V · 2005 to 2009
$7.1M
Intramural NIH HHSNIAID NIH HHS AI36214NIAID NIH HHS P30 AI036214NIAID NIH HHS U19 AI065664NIGMS NIH HHS T32 GM007198NIMH NIH HHS P30 MH062512
6 · The paper itself

Abstract

backgroundPlasmodium falciparum infection induces human immunodeficiency virus (HIV) replication and accelerates a decline in CD4(+) T-cell count. The mechanisms contributing to these interactions have not been fully elucidated.

methodsWe infected peripheral blood mononuclear cells (PBMCs) with HIV type 1 (HIV-1) and then cocultured them with P. falciparum-infected red blood cells (iRBCs) or uninfected RBCs (uRBCs). Levels of HIV-1 p24 antigen and activation-associated cytokines were measured in culture supernatants. T-cell surface activation was assessed by flow cytometry.

resultsIt has been reported that iRBCs increase HIV replication, compared with uRBCs; that neutralizing tumor necrosis factor α (TNF-α) abrogates this increase; and that hemozoin enhances HIV production. In this study, we confirmed that TNF-α plays an important role in this interaction. We show that iRBCs increased CD4(+) T-cell expression of HLA-DR(+)/CD38(+) (P = .001), that monocyte/macrophage depletion reduced HIV production by 40%-50% (P < .001), and that hemozoin-laden monocytes/macrophages that were preincubated with iRBCs also stimulated HIV production.

conclusionsiRBCs activate CD4(+) T cells and stimulate HIV replication in a TNF-α-dependent manner following malarial antigen processing by monocytes/macrophages. These results suggest that the persistent elevation of HIV replication during and after acute bouts of P. falciparum malaria may be due, at least in part, to ongoing stimulation of CD4(+) T cells by hemozoin-loaded antigen-presenting cells within lymphoid tissues.

Indexed as

PhagocytosisVirus ReplicationAntigen-Presenting CellsCoculture TechniquesCulture MediaCytokinesHIV-1HIV Core Protein p24HumansPhagocytesPlasmodium falciparumCulture MediaCytokinesHIV Core Protein p24co-infectionHIVinteractionmalariamechanism of increased viral loadP. falciparum

Identifiers

PMID24903666
PMCPMC4215075
OpenAlexW2118296432

What OpenQuestion holds

Textmetadata
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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.