ArticlemBio2026
A CDK-4EBP1 signaling axis drives HSV-1 replication and underscores a druggable pathway for potent antiviral intervention.
Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) poses a persistent public health challenge, particularly due to the emergence of drug-resistant strains and the limited efficacy of current monotherapies. Through an unbiased multi-omic approach, we identify a previously lesser-known viral strategy in which HSV-1 hijacks cyclin-dependent kinase (CDK) signaling to disrupt host cell cycle and translational control, specifically via the eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1). Targeted knockdown of CDKs confirmed their critical role in mediating 4EBP1 dephosphorylation during infection. Mechanistic evaluation of BX795, a previously known modulator of the 4EBP1 pathway, revealed an alternative route of translational repression mediated through CDKs. To further support this conclusion, we demonstrated that a distinct small-molecule CDK inhibitor, GW8510, exhibits potent antiviral activity against HSV-1 and functions as a true mechanistic analog of BX795. Together, these findings uncover a previously unrecognized CDK-4EBP1 regulatory axis exploited by HSV-1 and identify GW8510 as a promising candidate for host-directed antiviral intervention.IMPORTANCEHerpes simplex virus type 1 remains a major clinical burden, and resistance to existing therapies underscores the need for alternative strategies. This study reveals a mechanism by which HSV-1 regulates host cell cycle and translation control through cyclin-dependent kinase signaling and the 4E-binding protein 1 pathway. By revealing that pharmacological inhibition of this pathway suppresses viral replication, we identify a host-directed therapeutic approach that circumvents challenges associated with viral resistance to the current drugs. The demonstration of potent antiviral activity by GW8510, a small-molecule cyclin-dependent kinase inhibitor, establishes a promising foundation for translational development and highlights the potential of targeting host regulatory networks to combat viral infection.
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Registered trials
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.