Evidence map›Paper›PMID 42640959›Full record

ArticlePLoS pathogens2026

A multi-omics approach reveals specific oncogenic and inflammatory potential of viral oncoproteins Tax from neglected HTLV-1b and -1c genotypes.

Thomas Duchateau, Alice Bongers, Karim Abdelmoumen, Carine Rey, Sébastien Dussurgey, Jacques Brocard, Dalia Gerardin, Marie-Lou Béziat, Florence Lormières, Devashish Bhat and 4 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Thomas DuchateauCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.
Alice BongersUnité Épidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, Université Paris Cité, Paris, France.
Karim AbdelmoumenCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.
Carine ReyCentre International de Recherche en Infectiologie, BioInformatic and BioStatistics Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.
Sébastien DussurgeyUniversite Claude Bernard Lyon 1, CNRS UAR3444, Inserm US8, ENS de Lyon, SFR Biosciences, Lyon, France.
Jacques BrocardUniversite Claude Bernard Lyon 1, CNRS UAR3444, Inserm US8, ENS de Lyon, SFR Biosciences, Lyon, France.
Dalia GerardinCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.
Marie-Lou BéziatCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.
Florence LormièresCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.
Devashish BhatCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.ORCID 0009-0000-6352-503X
Christophe GuillonMolecular Microbiology and Structural Biochemistry, Retroviruses and Structural Biochemistry Team, CNRS UMR5086, Université Claude Bernard Lyon 1, Lyon, France.
Patrice GouetMolecular Microbiology and Structural Biochemistry, Retroviruses and Structural Biochemistry Team, CNRS UMR5086, Université Claude Bernard Lyon 1, Lyon, France.
Philippe V AfonsoUnité Épidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, Université Paris Cité, Paris, France.
Chloé JournoCentre International de Recherche en Infectiologie, Retroviral Oncogenesis Team, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.ORCID 0000-0002-0973-0777

Funding

Agence Nationale de la Recherche, FranceNormale Supérieure de Lyon, France
6 · The paper itself

Abstract

Over the recent years, reports of very high prevalence of Human T-cell Leukemia Virus (HTLV) type 1 genotype c infection in remote aboriginal populations in Central Australia have sparked a renewed interest in the genetic variability of this human oncogenic retrovirus. While clinical and epidemiological studies suggest that HTLV-1 genotypes might be associated with varying risks of pathological manifestations, molecular comparisons of the viral determinants among genotypes remain scarce. In this study, we provide the first comprehensive comparative analysis of the major oncoprotein Tax1 from genotypes a (Japanese), b (African) and c (Australo-Melanesia). Using unbiased analysis of image cytometry data from Tax1-expressing Jurkat T-cells, combined with proximity labelling, we first show that Tax1 variants exhibit distinct subcellular localization in T-cells. Indeed, in contrast to Tax1a that assembles a NF-κB-activating signalosome associated with the Golgi apparatus, Tax1c variants lack any significant association with this cell compartment. Surprisingly however, Tax1c does not show any general defect in NF-κB activation compared to Tax1a and Tax1b. Nevertheless, transcriptomics analysis combined with pathway inference indicate that the quality of the NF-κB signature induced by Tax1c differs from that of Tax1a, and that the transcriptional landscape of Tax1c-expressing cells is biased towards T-cell activation and inflammation, an observation that is consistent with the kinome profiling of Tax1c-expressing cells. Analysis of Tax1b-induced transcriptional reprogramming revealed that it closely parallels that of Tax1a, but with a higher magnitude. In addition, distinct modulation of cell cycle-related kinase activity by Tax1b compared to Tax1a was correlated with a specific modulation of the cell cycle. Consistently, functional cell transformation assays demonstrated that Tax1b presents a higher oncogenic potential compared to Tax1a, while Tax1c harbours a decreased transforming activity. Altogether, we provide evidence of functional divergence among Tax1 from different genotypes that may have pathophysiological and clinical implications.

Indexed as

Gene Products, taxHTLV-I InfectionsHuman T-lymphotropic virus 1GenotypeHumansInflammationJurkat CellsNF-kappa BGene Products, taxNF-kappa Btax protein, Human T-lymphotrophic virus 1

Identifiers

PMID42640959
PMCPMC13537692

What Socratic holds

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Registered trials

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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 Socratic graph.