Evidence map›Paper›PMID 41617085›Full record

ArticleVirologica Sinica2026

Pseudorabies virus TK protein antagonizes alpha interferon response by interfering with the JAK1-STAT1 interaction.

Jingjing Song, Rulan Bai, Dongyue Xing, Chuang Li, Xuan Chen, Feiyang Zheng, Mingyi Lei, Yujin Wang, Yuxin Liu, Jun Tang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virologica Sinica, 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.

Jingjing SongState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Rulan BaiState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Dongyue XingState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Chuang LiState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Xuan ChenState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Feiyang ZhengState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Mingyi LeiState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Yujin WangState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Yuxin LiuState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Jun TangState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Pinghuang LiuState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Changyong ChengKey Laboratory of Applied Biotechnology on Animal Science & Veterinary Medicine of Zhejiang Province, College of Veterinary Medicine of Zhejiang A&F University, Hangzhou 311300, China.
Jin YuanCollege of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China. Electronic address: yuanjin@henau.edu.cn.
Rui ZhangState Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China. Electronic address: 2015001@cau.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudorabies virus (PRV), a member of the Alphaherpesvirinae subfamily, is the causative agent of Aujeszky's disease, which severely affects swine health and poses a potential zoonotic risk. PRV can evade the type I interferon (IFN-I)-mediated antiviral response, thus enabling persistent infection, yet the molecular basis for this immune evasion remains unclear. Here, we identify a novel role for thymidine kinase (TK), a key PRV virulence factor, in suppressing IFN-I signaling. Ectopic expression of TK markedly inhibited IFNα-induced transcription and expression of interferon-stimulated genes (ISGs), whereas TK-deficient PRV (PRV-ΔTK) showed increased sensitivity to IFN-I, elevated ISG expression, and reduced replication following IFNα treatment. Mechanistic analyses revealed that TK interacts with both Janus kinase 1 (JAK1) and signal transducer and activator of transcription 1 (STAT1), disrupting the JAK1-STAT1 complex formation and impairing STAT1 phosphorylation and downstream ISG induction. This inhibition is mediated by amino acids 107-212 of TK, a region independent of its catalytic site, and is essential for its immunosuppressive activity. These findings uncover a previously unrecognized function of TK in antagonizing the IFN-I response through interference with JAK1-STAT1 signaling. Beyond its established role in nucleotide metabolism and virulence, this immune evasion function may account for the strong conservation of TK among PRV strains. Collectively, our results expand the understanding of PRV pathogenesis and identify TK as a potential target for antiviral intervention.

Indexed as

Herpesvirus 1, SuidInterferon-alphaJanus Kinase 1STAT1 Transcription FactorThymidine KinaseViral ProteinsAnimalsCell LineHumansImmune EvasionProtein BindingPseudorabiesSignal TransductionSwineInterferon-alphaJanus Kinase 1STAT1 Transcription FactorThymidine KinaseViral ProteinsIFN signaling pathwayJAK1Pseudorabies virus (PRV)STAT1Thymidine kinase (TK)

Identifiers

PMID41617085
PMCPMC13007314

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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.