Evidence map›Paper›PMID 39869648›Full record

ArticlePLoS pathogens2025

M-Sec promotes the accumulation of intracellular HTLV-1 Gag puncta and the incorporation of Env into viral particles.

Masateru Hiyoshi, Youssef M Eltalkhawy, Randa A Abdelnaser, Akira Ono, Kazuaki Monde, Yosuke Maeda, Reem M Mahmoud, Naofumi Takahashi, Yasuyoshi Hatayama, Akihide Ryo and 4 more

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Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

14 authors.

Masateru HiyoshiResearch Center for Biological Products in the Next Generation, National Institute of Infectious Diseases, Tokyo, Japan.
Youssef M EltalkhawyJoint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Randa A AbdelnaserJoint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Akira OnoDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Kazuaki MondeDepartment of Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yosuke MaedaDepartment of Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Reem M MahmoudJoint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Naofumi TakahashiJoint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Yasuyoshi HatayamaDepartment of Virology III, National Institute of Infectious Diseases, Tokyo, Japan.
Akihide RyoDepartment of Virology III, National Institute of Infectious Diseases, Tokyo, Japan.
Satoshi NozumaDepartment of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Hiroshi TakashimaDepartment of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Ryuji KubotaJoint Research Center for Human Retrovirus Infection, Kagoshima University, Kagoshima, Japan.
Shinya SuzuJoint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.ORCID 0000-0003-2531-4770

Funding

Mechanisms that determine subcellular sites of HIV-1 assemblyR37AI071727 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Akira Ono · 2017 to 2026
$6.2M
NIAID NIH HHS R37 AI071727
6 · The paper itself

Abstract

We have demonstrated that the cellular protein M-Sec promotes the transmission of human T-cell leukemia virus type 1 (HTLV-1) in vitro and in vivo. Here, we show how HTLV-1 utilizes M-Sec for its efficient transmission. HTLV-1-infected CD4+ T cells expressed M-Sec at a higher level than uninfected CD4+ T cells. The ex vivo culture of the infected cells upregulated the expression of M-Sec, the level of which was sustained for a long time. The viral structural protein Gag is distributed in a punctate pattern in cells. M-Sec promoted the accumulation of large intracellular Gag puncta. This accumulation was dependent on phosphatidylinositol 4,5-bisphosphate (PIP2), since it was lost upon the removal of PIP2 binding motifs in M-Sec or the depletion of cellular PIP2. The viral envelope protein Env co-localized with the large Gag puncta induced by M-Sec. Furthermore, viral particles produced by M-Sec-expressing cells contained a higher amount of Env. Given that M-Sec alters the cellular distribution of PIP2, these results suggest that M-Sec promotes the formation of infectious viral particles through PIP2. Since the expression of M-Sec is mediated by HTLV-1 Tax protein, M-Sec appears to function in a positive feedback loop that ensures efficient HTLV-1 transmission.

Indexed as

Gene Products, envGene Products, gagHTLV-I InfectionsHuman T-lymphotropic virus 1VirionCD4-Positive T-LymphocytesHumansPhosphatidylinositol 4,5-DiphosphateGene Products, envGene Products, gagPhosphatidylinositol 4,5-Diphosphate

Identifiers

PMID39869648
PMCPMC11801699

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.