Evidence map›Paper›PMID 32615983›Full record

ArticleRetrovirology2020

HIV-1 subtype C transmitted founders modulate dendritic cell inflammatory responses.

Evelyn Ngwa Lumngwena, Simon Metenou, Lindi Masson, Claudia Cicala, James Arthos, Zenda Woodman

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

Article in Retrovirology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Immuno-cell metabolic changes in HIV-1 infection.Infectious diseases & immunity · 2025
    Review
  2. 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 4 countries.

Evelyn Ngwa LumngwenaDivision of Cardiology, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. lumngwena@yahoo.co.uk.
Simon MetenouNational Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, USA.
Lindi MassonDisease Elimination Program, Life Sciences Discipline, Burnet Institute, Melbourne, Australia.
Claudia CicalaNational Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, USA.
James ArthosNational Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, USA.
Zenda WoodmanDepartment of Integrative Biomedical Sciences (IBMS), Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. Zl.woodman@uct.ac.za.ORCID 0000-0001-9680-3884
National Institute of Allergy and Infectious Diseases · USUniversity of Cape Town · ZABurnet Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeterosexual transmission remains the main route of HIV-1 transmission and female genital tract (FGT) inflammation increases the risk of infection. However, the mechanism(s) by which inflammation facilitates infection is not fully understood. In rhesus macaques challenged with simian immunodeficiency virus, dendritic cell (DC) mediated recruitment of CD4+ T cells to the FGT was critical for infection. The aim of this study was to delineate the mechanisms underlying DC-mediated HIV infection by comparing chemokine and pro-inflammatory cytokine production in response to transmitted founder (TF) and chronic infection (CI) Envelope (Env) pseudotyped viruses (PSV).

resultsMonocyte-derived DCs (MDDCs) were stimulated with PSV and recombinant gp140 representing matched TF and CI pairs of four individuals and cytokine secretion measured by multiplex immuno-assay. We found that 4/9 Env induced robust MDDC inflammatory responses and of those, three were cloned from TFs. Overall, TF Env induced MDDCs from healthy donors to secrete higher concentrations of inflammatory cytokines and chemokines than those from CI, suggesting TF Env were better inducers of inflammation. Assessing the signalling pathway associated with inflammatory cytokines, we found that PSV of matched TF and CI variants and a gp140 clone activated ERK and JNK to similar levels. Recombinant soluble DC-SIGN inhibited cytokine release and activation of ERK by PSV, suggesting that Env-DC-SIGN binding was partly involved in MDDC stimulation. Therefore, Env clones might differentially stimulate MDDC immune responses via alternative, yet unidentified signalling pathways.

conclusionOverall, this could suggest that the genetics of the virus itself influences inflammatory responses during HIV infection. In the absence of pre-existing infections, induction of greater inflammatory response by TFs might favour virus survival within the healthy FGT by driving an influx of target cells to sites of infection while suppressing immune responses via IL-10.

Indexed as

Cell Adhesion MoleculesChemokinesCytokinesDC-Specific ICAM-3 Grabbing NonintegrinDendritic Cellsenv Gene Products, Human Immunodeficiency VirusFemaleHIV-1HIV InfectionsHumansLectins, C-TypeMitogen-Activated Protein Kinase KinasesMonocytesReceptors, Cell SurfaceSignal TransductionCell Adhesion MoleculesChemokinesCytokinesDC-Specific ICAM-3 Grabbing Nonintegrinenv Gene Products, Human Immunodeficiency Virusgp140 envelope protein, Human immunodeficiency virus 1Lectins, C-TypeMitogen-Activated Protein Kinase KinasesReceptors, Cell SurfaceHIV-subtype C EnvImmunosuppressionInflammatory responsesTransmissionTransmitter/Founder EnvelopesVirus survival

Identifiers

PMID32615983
PMCPMC7331269
OpenAlexW3040211080

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.