Evidence map›Paper›PMID 40370235›Full record

ArticleCurrent molecular medicine2026

Boosting Antiviral Defenses: stat3 Inhibition Enhances Type I Interferon Response to Respiratory Syncytial Virus by Silencing KAP1.

Huagui Chen, Dongmei Ding, Zimeng Teng, Ran Zhang

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Article in Current molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Huagui ChenHunan Normal University Health Science Center, Changsha, China.
Dongmei DingClinical Laboratory, Nanning Aier Eye Hospital, 371, Tongzipo Road, Changsha, 410013, Hunan, China.
Zimeng TengHunan Normal University Health Science Center, Changsha, China.
Ran ZhangHunan Normal University Health Science Center, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe antiviral effects of type I interferons [IFNs] on respiratory syncytial virus [RSV]-infected airway epithelial cells have been identified. We aim to further reveal the mechanism of stat3 and kruppel-associated box-associated protein 1 [KAP1] in RSV-infected airway epithelial cells.

methodsUsing the A549 cell line, we investigated the impact of RSV infection, KAP1 overexpression, and stat3 inhibition with Stattic. Cell counting kit 8 assay was used to determine the viability, and enzyme-linked immunosorbent assay was applied to measure the levels of IL-6, IL-8, IL-1β, IFN-α, and IFN-β. Viral replication was tested via plaque assay. Meanwhile, quantitative real-time reverse transcription polymerase chain reaction or/and western blot were applied to measure the expressions of p-stat3 and KAP1 in the cells. RESULTS AND DISCUSSION: RSV infection repressed the viability, upregulated p-stat3 and KAP1 expressions, elevated levels of inflammation-related factors [IL-6, IL-8, IL- 1β], and type I IFN immune response-associated factors [IFN-α, IFN-β], and promoted viral replication in A549 cells. Stattic attenuated the promoting effect of RSV on inflammation-related factors and viral replication, but enhanced its impact on IFN-α and IFN-β levels in the cells. More importantly, KAP1 overexpression reversed the effects of Stattic on viability, inflammation [IL-6, IL-8, IL-1β], type I IFN immune response [IFN-α, IFN-β], and viral replication in RSV-infected A549 cells.

conclusionOur findings unveil the pivotal role of stat3 inhibition in potentiating type I IFN-mediated antiviral responses against RSV in lung epithelial cells, revealing KAP1 as a potential therapeutic target for combating respiratory viral infections.

Indexed as

Interferon Type IRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsSTAT3 Transcription FactorTripartite Motif-Containing Protein 28A549 CellsGene SilencingHumansVirus ReplicationInterferon Type ISTAT3 protein, humanSTAT3 Transcription FactorTRIM28 protein, humanTripartite Motif-Containing Protein 28immune responsekruppel-associated box-associated protein 1lung epithelial cellsrespiratory syncytial virusSignal transducer and activator of transcription 3Stattictype I interferon

Identifiers

PMID40370235

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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.