tetano
Editor, Senior Moderator
Virus Genes
. 2025 Jul 3.
doi: 10.1007/s11262-025-02173-z. Online ahead of print. ARF3 knockdown inhibits influenza a virus and virus-induced pneumonia
Zhinan Zhang[SUP] 1 [/SUP], Banghao Lu[SUP] 2 [/SUP], Bihe Zeng[SUP] 3 [/SUP]
Affiliations
Pneumonia, characterized by infection-induced inflammation of the lungs, poses a significant health burden, particularly among children. ADP ribosylation factor 3 (ARF3) is a key regulatory protein implicated in various pathological processes; however, its role in pneumonia caused by influenza A virus (IAV) remains inadequately understood. In this study, we demonstrated that ARF3 expression was upregulated in a young mouse model of IAV-induced pneumonia. Knockdown of ARF3 effectively mitigated lung injury in this model. Furthermore, suppression of ARF3 expression alleviated pulmonary inflammation by reducing the levels of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β. In vitro experiments further revealed that ARF3 downregulation inhibited replication of the H3N2 IAV strain. Notably, ARF3 knockdown also attenuated NLRP3 inflammasome activation, a key mediator of inflammatory responses. Collectively, these findings provide the first evidence that ARF3 knockdown suppresses both IAV replication and virus-induced pneumonia by modulating inflammasome activation, suggesting that ARF3 may serve as a potential therapeutic target for pneumonia intervention.
Keywords: ARF3; IAV; NLRP3 inflammasome; Pneumonia.
. 2025 Jul 3.
doi: 10.1007/s11262-025-02173-z. Online ahead of print. ARF3 knockdown inhibits influenza a virus and virus-induced pneumonia
Zhinan Zhang[SUP] 1 [/SUP], Banghao Lu[SUP] 2 [/SUP], Bihe Zeng[SUP] 3 [/SUP]
Affiliations
- PMID: 40608252
- DOI: 10.1007/s11262-025-02173-z
Pneumonia, characterized by infection-induced inflammation of the lungs, poses a significant health burden, particularly among children. ADP ribosylation factor 3 (ARF3) is a key regulatory protein implicated in various pathological processes; however, its role in pneumonia caused by influenza A virus (IAV) remains inadequately understood. In this study, we demonstrated that ARF3 expression was upregulated in a young mouse model of IAV-induced pneumonia. Knockdown of ARF3 effectively mitigated lung injury in this model. Furthermore, suppression of ARF3 expression alleviated pulmonary inflammation by reducing the levels of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β. In vitro experiments further revealed that ARF3 downregulation inhibited replication of the H3N2 IAV strain. Notably, ARF3 knockdown also attenuated NLRP3 inflammasome activation, a key mediator of inflammatory responses. Collectively, these findings provide the first evidence that ARF3 knockdown suppresses both IAV replication and virus-induced pneumonia by modulating inflammasome activation, suggesting that ARF3 may serve as a potential therapeutic target for pneumonia intervention.
Keywords: ARF3; IAV; NLRP3 inflammasome; Pneumonia.