Evidence map›Paper›PMID 41754420›Full record

ArticlePathogens (Basel, Switzerland)2026

PIM1 and PIM3 Kinases Suppress HIV-1 Protein Expression and Particle Production Through Distinct Roles.

Khanh Quoc Tran, Bao Quoc Le, Takaaki Koma, Naoya Doi, Tomoyuki Kondo, Nanako Komoda, Mei Udagawa, Nozomi Okumura, Chisato Gotoda, Mari Nagasaka and 4 more

Abstract read
In one paragraph

Article in Pathogens (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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.

Khanh Quoc TranDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.ORCID 0009-0008-4023-756X
Bao Quoc LeDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.ORCID 0009-0004-4811-2025
Takaaki KomaDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.ORCID 0000-0001-9767-990X
Naoya DoiDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Tomoyuki KondoDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Nanako KomodaFaculty of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Mei UdagawaFaculty of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Nozomi OkumuraFaculty of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Chisato GotodaFaculty of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Mari NagasakaFaculty of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Takumi IchinomiyaFaculty of Medicine, Tokushima University, Tokushima 770-8503, Japan.
Yuma InamotoTransdisciplinary Program for Medicine, Photonics, and Engineering, Faculty of Science and Technology, Tokushima University, Tokushima 770-0813, Japan.
Akio AdachiDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.ORCID 0000-0003-1674-332X
Masako NomaguchiDepartment of Microbiology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.

Funding

Japan Society for the Promotion of Science 24K0249300Japan Society for the Promotion of Science 24K1165500Japan Society for the Promotion of Science 25K1175800
6 · The paper itself

Abstract

PIM kinases (PIM1, PIM2, PIM3) are serine/threonine kinases implicated in infection and reactivation of various viruses, but their roles in HIV-1 gene expression and particle production remain unclear. We examined their impact on HIV-1 and related viruses using co-transfection systems. PIM1 and PIM3, but not PIM2, markedly suppressed HIV-1 virion production without affecting infectivity. This inhibitory effect extended to transmitted/founder HIV-1 clones and SIV, indicating broad activity across lentiviruses. Kinase-dead mutants failed to reduce virion production, confirming the requirement for catalytic activity. Our data suggest that PIM1 and PIM3 act at distinct steps of HIV-1 gene expression: PIM1 reduces transcription, whereas PIM3 acts post-transcriptionally to diminish viral protein expression. Co-expression of PIM1 and PIM3 further enhanced suppression, suggesting complementary functions. Both kinases also inhibited expression from non-LTR promoters, implying involvement of general cellular factors. These findings reveal distinct and cooperative actions of PIM1 and PIM3 in limiting HIV-1 particle production, providing new insights into host kinase-mediated regulation of viral gene expression.

Indexed as

Gene Expression Regulation, ViralHIV-1HIV InfectionsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1VirionCell LineHost-Pathogen InteractionsHumansVirus ReplicationPIM1 protein, humanPIM3 protein, humanProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1gene expressionHIV-1Host–virus interactionPIM kinasesvirion production

Identifiers

PMID41754420
PMCPMC12943119

What Socratic holds

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LicenceCC BY
Read underepoch 390

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.