Evidence map›Paper›PMID 30563084›Full record

ReviewViruses2018

Cytokine Networks Dysregulation during HTLV-1 Infection and Associated Diseases.

Nicolas Futsch, Gabriela Prates, Renaud Mahieux, Jorge Casseb, Hélène Dutartre

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 85 citations in OpenAlex.

  1. Dolutegravir Reduces Human T-Cell Lymphotropic Virus Type 1 Proviral Load and Improves Neurological Outcomes in a Phase 2 Controlled Trial.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026
    Trial
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  10. Review
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  13. Observational
  14. Complete Rescue of HTLV-1Pathogens (Basel, Switzerland) · 2024
    Article
  15. Review
  16. Article
  17. Article
  18. 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

5 authors at 2 institutions in 2 countries.

Nicolas FutschÉquipe Oncogenèse Rétrovirale, Equipe Labellisée «FRM», CIRI-Centre International de Recherche en Infectiologie, Université Claude Bernard Lyon 1, Inserm U1111, CNRS UMR5308, Labex Ecofect, ENS Lyon, F-69007 Lyon, France. nicolas.futsch@ens-lyon.fr.
Gabriela PratesInstitute of Tropical Medicine of São Paulo, São Paulo, SP 05403-000, Brazil. gabrielaprates12@hotmail.com.ORCID 0000-0003-3728-9621
Renaud MahieuxÉquipe Oncogenèse Rétrovirale, Equipe Labellisée «FRM», CIRI-Centre International de Recherche en Infectiologie, Université Claude Bernard Lyon 1, Inserm U1111, CNRS UMR5308, Labex Ecofect, ENS Lyon, F-69007 Lyon, France. renaud.mahieux@ens-lyon.fr.ORCID 0000-0002-5129-6804
Jorge CassebInstitute of Tropical Medicine of São Paulo, São Paulo, SP 05403-000, Brazil. jcasseb10@gmail.com.ORCID 0000-0002-4553-2559
Hélène DutartreÉquipe Oncogenèse Rétrovirale, Equipe Labellisée «FRM», CIRI-Centre International de Recherche en Infectiologie, Université Claude Bernard Lyon 1, Inserm U1111, CNRS UMR5308, Labex Ecofect, ENS Lyon, F-69007 Lyon, France. helene.dutartre@ens-lyon.fr.ORCID 0000-0002-2682-4302
Université Claude Bernard Lyon 1 · FRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a neural chronic inflammation, called HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and of a malignant lymphoproliferation, called the adult T-cell leukemia/lymphoma (ATLL). The mechanisms through which the HTLV-1 induces these diseases are still unclear, but they might rely on immune alterations. HAM/TSP is associated with an impaired production of pro-inflammatory cytokines and chemokines, such as IFN-γ, TNF-α, CXCL9, or CXCL10. ATLL is associated with high levels of IL-10 and TGF-β. These immunosuppressive cytokines could promote a protumoral micro-environment. Moreover, HTLV-1 infection impairs the IFN-I production and signaling, and favors the IL-2, IL-4, and IL-6 expression. This contributes both to immune escape and to infected cells proliferation. Here, we review the landscape of cytokine dysregulations induced by HTLV-1 infection and the role of these cytokines in the HTLV-1-associated diseases progression.

Indexed as

Signal TransductionAnimalsChemokine CXCL9ChemokinesCytokinesHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Interferon-gammaInterleukin-10Leukemia-Lymphoma, Adult T-CellMiceParaparesis, Tropical SpasticTumor Necrosis Factor-alphaChemokine CXCL9ChemokinesCXCL9 protein, humanCytokinesIL10 protein, humanInterferon-gammaInterleukin-10Tumor Necrosis Factor-alphaATLLcytokinesHAM/TSPHTLV-1immune system

Identifiers

PMID30563084
PMCPMC6315340
OpenAlexW2902960775

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.