Intervirology · 2026
Formulated Curcumin Exerts Potent Anti-Influenza Activity by Inhibition of Akt Activation and Viral Genome Replication.
СтатьяНазвание и аннотация: Перевод в очереди
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Chang Hui-Ming, Lai Ping-Shan, Li Cun-Zhao, Lin Fong-Yuan, Chen Da-Yuan, Tsai Ruei-Sheng, Ou Shan-Chia, Ma Nianhan, Hsu Wei-Li
Аннотация
INTRODUCTION: Influenza A viruses (IAVs) cause not only seasonal epidemics but also pandemics in humans. The emergence of H5N1 variants resistant to oseltamivir highlights the need to develop new antiviral therapeutic strategies. Accumulated evidence has indicated the potent anti-influenza activity of curcumin (Cur). Nevertheless, the unsatisfactory bioavailability of Cur limits its clinical use.
METHODS: In the present study, the anti-influenza activity and underlying mechanism of encapsulated Cur in nanoparticle form, referred to as Cur-micelle (Cur-M), were evaluated.
RESULTS: Our results demonstrated that, as with native Cur treatment, Cur-M treatment remarkably reduced IAV infection. Interestingly, Cur-M significantly inhibited IAV infectivity post-viral entry, while treatment with Cur alone showed no effect, as demonstrated by differences in plaque formation ability. By monitoring intracellular processing, including the signaling pathway required for IAV propagation and the critical viral replication step, we discovered that viral RNA replication and the activation of Akt signaling were significantly suppressed under Cur-M treatment.
CONCLUSION: This study demonstrates for the first time that Cur-M interferes with intracellular processes required for influenza virus infection, highlighting its potential for further evaluation in both cell-based and in vivo systems.
METHODS: In the present study, the anti-influenza activity and underlying mechanism of encapsulated Cur in nanoparticle form, referred to as Cur-micelle (Cur-M), were evaluated.
RESULTS: Our results demonstrated that, as with native Cur treatment, Cur-M treatment remarkably reduced IAV infection. Interestingly, Cur-M significantly inhibited IAV infectivity post-viral entry, while treatment with Cur alone showed no effect, as demonstrated by differences in plaque formation ability. By monitoring intracellular processing, including the signaling pathway required for IAV propagation and the critical viral replication step, we discovered that viral RNA replication and the activation of Akt signaling were significantly suppressed under Cur-M treatment.
CONCLUSION: This study demonstrates for the first time that Cur-M interferes with intracellular processes required for influenza virus infection, highlighting its potential for further evaluation in both cell-based and in vivo systems.