tetano
Editor, Senior Moderator
J Med Virol
. 2020 Aug 10.
doi: 10.1002/jmv.26403. Online ahead of print.
Apigenin suppresses influenza A virus-induced RIG-I activation and viral replication
Xiaohong Xu[SUP] 1 [/SUP], Jing Miao[SUP] 2 [/SUP], Qingliang Shao[SUP] 1 [/SUP], Yue Gao[SUP] 1 [/SUP], Luojia Hong[SUP] 3 [/SUP]
Affiliations
Abstract
Apigenin is a flavonoid of low toxicity and multiple beneficial bioactivities, including the properties of antitumor, antioxidant, anti-inflammatory and antiviral activities. However, the effects of Apigenin on influenza virus infection remain poorly understood. Thus, the aim of this study is to investigate the effect of Apigenin on influenza A virus (IAV)-induced inflammation and viral replication. This study demonstrated that Apigenin treatment significantly suppressed IAV-induced upregulation of RIG-I expression, as well as the production of pro-inflammatory cytokines and interferons (IFN-β and IFN-λ1). Meanwhile, Apigenin also protected cell from IAV-induced cell death. In addition, Apigenin specifically inhibited the activation of RIG-I signaling via promoting the ubiquitin-mediated degradation of RIG-I, which may cause by the disrupting its interaction with Hsp90α. Interestingly, instead of enhancing viral replication due to the inhibitory effects of Apigenin on the activation of RIG-I and expression of IFNs, Apigenin inhibited IAV replication in vitro. Further study demonstrated that Apigenin inhibited the influenza viral neuraminidase (NA) activity. Thus, Apigenin may serve as a promising supplementary approach for treatment of influenza because it protected cell from IAV-induced cell death and inhibited viral NA activity to suppress viral replication. This article is protected by copyright. All rights reserved.
Keywords: Apigenin; RIG-I; influenza A virus; viral replication.
. 2020 Aug 10.
doi: 10.1002/jmv.26403. Online ahead of print.
Apigenin suppresses influenza A virus-induced RIG-I activation and viral replication
Xiaohong Xu[SUP] 1 [/SUP], Jing Miao[SUP] 2 [/SUP], Qingliang Shao[SUP] 1 [/SUP], Yue Gao[SUP] 1 [/SUP], Luojia Hong[SUP] 3 [/SUP]
Affiliations
- PMID: 32776519
- DOI: 10.1002/jmv.26403
Abstract
Apigenin is a flavonoid of low toxicity and multiple beneficial bioactivities, including the properties of antitumor, antioxidant, anti-inflammatory and antiviral activities. However, the effects of Apigenin on influenza virus infection remain poorly understood. Thus, the aim of this study is to investigate the effect of Apigenin on influenza A virus (IAV)-induced inflammation and viral replication. This study demonstrated that Apigenin treatment significantly suppressed IAV-induced upregulation of RIG-I expression, as well as the production of pro-inflammatory cytokines and interferons (IFN-β and IFN-λ1). Meanwhile, Apigenin also protected cell from IAV-induced cell death. In addition, Apigenin specifically inhibited the activation of RIG-I signaling via promoting the ubiquitin-mediated degradation of RIG-I, which may cause by the disrupting its interaction with Hsp90α. Interestingly, instead of enhancing viral replication due to the inhibitory effects of Apigenin on the activation of RIG-I and expression of IFNs, Apigenin inhibited IAV replication in vitro. Further study demonstrated that Apigenin inhibited the influenza viral neuraminidase (NA) activity. Thus, Apigenin may serve as a promising supplementary approach for treatment of influenza because it protected cell from IAV-induced cell death and inhibited viral NA activity to suppress viral replication. This article is protected by copyright. All rights reserved.
Keywords: Apigenin; RIG-I; influenza A virus; viral replication.