Evidence map›Paper›PMID 42224353›Full record

ArticlePLoS pathogens2026

M-Sec promotes the production of infectious HIV-1 virus through the exocyst complex in macrophages.

Reem M Mahmoud, Masateru Hiyoshi, Randa A Abdelnaser, Kazuaki Monde, Nami Monde, Takaaki Koma, Hidenobu Mizuno, Sara A Habash, Naofumi Takahashi, Yosuke Maeda and 2 more

Abstract read
PubMed Full text at PMC Publisher
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. 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

5 · Who and what money

Authors and funding

12 authors.

Reem M MahmoudDivision of Infection & Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Masateru HiyoshiCenter for Next-Generation Biologics Research, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Randa A AbdelnaserDivision of Infection & Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Kazuaki MondeDepartment of Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Nami MondeDepartment of Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Takaaki KomaDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Hidenobu MizunoInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.
Sara A HabashDivision of Infection & Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Naofumi TakahashiDivision of Infection & Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Yosuke MaedaDepartment of Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Akira OnoDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Shinya SuzuDivision of Infection & Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0003-2531-4770

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have demonstrated that the cellular protein M-Sec promotes the transmission of human immunodeficiency virus type 1 (HIV-1) in macrophages. However, the underlying mechanism is not fully understood. Here, we report that M-Sec promotes the production of infectious HIV-1 virus. The major viral structural protein Gag distributed as many puncta in infected cells, which is one of the indicators of viral particle formation. The knockdown of M-Sec hindered the Gag puncta formation and co-localization of Gag with the viral envelope protein Env in cells, and reduced the amount of Env and infectivity of the produced virus. Consistent with these results, the over-expression of M-Sec induced the accumulation of Gag puncta, Gag/Env co-localization, and Env incorporation into virus and viral infectivity. M-Sec is known to bind phosphatidylinositol 4,5-bisphosphate (PIP2) and a small GTPase Ral, both of which were required for the M-Sec-mediated HIV-1 regulation. The exocyst complex, which is the downstream effector of Ral, was also required for the M-Sec-mediated HIV-1 regulation. Because PIP2, Ral and the exocyst complex are important for the M-Sec-mediated formation of the long plasma membrane protrusions, the present study suggests that M-Sec promotes HIV-1 transmission by acting on both cell structures and viral production through these overlapping components.

Indexed as

HIV-1HIV InfectionsMacrophagesVesicular Transport Proteinsenv Gene Products, Human Immunodeficiency Virusgag Gene Products, Human Immunodeficiency VirusHumansPhosphatidylinositol 4,5-Diphosphateral GTP-Binding ProteinsVirus Replicationenv Gene Products, Human Immunodeficiency VirusEXOC7 protein, humangag Gene Products, Human Immunodeficiency VirusPhosphatidylinositol 4,5-Diphosphateral GTP-Binding ProteinsVesicular Transport Proteins

Identifiers

PMID42224353
PMCPMC13235924

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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.