ArticleVeterinary research2025
The African swine fever virus B125R protein antagonizes JAK-STAT signalling by promoting the degradation of IFNAR2.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Review
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- Host-Microbe Interactions: Understanding the Mechanism of Autophagy in Viral Replication and Immune Evasion.Veterinary sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
African swine fever (ASF) is a highly contagious and severe hemorrhagic disease caused by African swine fever virus (ASFV). Currently, few safe and effective vaccines or antiviral drugs are available for its prevention. Interferon (IFN), a key component of innate antiviral immunity, induces interferon-stimulated genes (ISGs) by activating the JAK-STAT signalling pathway, resulting in antiviral effects. ASFV strains, including ASFV SY18, ASFV HLJ18, and ASFV BA71V, are highly sensitive to IFN-I treatment; however, the mechanisms by which ASFV antagonizes the host type I IFN response have not been fully elucidated. In this study, we identified the ASFV B125R protein (pB125R) as a negative regulator of the JAK-STAT pathway. We observed that ectopically expressed pB125R significantly suppressed the IFN-β-triggered activation of JAK-STAT signalling in HEK293T and PK-15 cells. Mechanistic studies revealed that pB125R binds to IFNAR2 and promotes its autophagic degradation, impairing the signal transduction of the IFN response at an early stage. This ultimately reduces the nuclear translocation of the ISGF3 complex and decreases ISG production. Our findings highlight the immunosuppressive activity of pB125R and reveal a novel mechanism by which ASFV evades the host IFN response, contributing to potential strategies for developing vaccines and therapeutics against ASF.
Indexed as
Identifiers
What OpenQuestion holds
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.