Apigenin suppresses influenza A virus-induced RIG-I activation and viral replication
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August 20, 2020

Apigenin suppresses influenza A virus-induced RIG-I activation and viral replication

By Matsuoka

Flavonoid apigenin is low toxicity and few favorable bioactivities, including anti-tumor properties, antioxidant, anti-inflammatory activity and antiviral. However, the effect of Apigenin on influenza virus infection remains poorly understood. Thus, the purpose of this study was to determine the effect of Apigenin on influenza A virus (IAV) induced inflammation and viral replication. This study showed that treatment significantly suppressed Apigenin IAV-induced upregulation of RIG-I expression, as well as the production of pro-inflammatory cytokines and interferon (IFN-β and IFN-λ1). Meanwhile, Apigenin also protected cells from IAV-induced cell death.

In addition, special Apigenin inhibits the activation of RIG-I signaling by promoting ubiquitin-mediated degradation of RIG-I, which can lead to disrupt the interaction with Hsp90α. Interestingly, not increase viral replication due to the inhibitory effect of Apigenin on RIG-I activation and the expression of IFN, Apigenin inhibited IAV replication in vitro. Further studies show that Apigenin inhibits viral neuraminidase (NA) of influenza activity. Thus, Apigenin may serve as a promising complementary approach to the treatment of influenza because the cells are protected from IAV-induced cell death and inhibits viral NA activity to suppress viral replication. This article is protected by copyright. All rights reserved.


In April 2009, a new influenza A virus (IAV) subtypes (A (H1N1) pdm09) scattered around the world and triggered the first human influenza pandemic of the 21st century. Since then, IAV exposure to pandemic H1N1 has been confirmed in different animal species. clinical and serological evidence of infection with the A (H1N1) have been reported in pdm09 canines, but the available information on the role of the dog in the epidemiology of this subtype IAV is still very limited in Europe. A cross-sectional study conducted to determine the seroprevalence A (H1N1) pdm09 in dogs in southern Spain, an area with seasonal circulation endemic in humans.

Sera collected from 750 canine companion during the period 2013-2016. Antibodies against H1N1 pandemic IAV analyzed using haemagglutination inhibition test. Positive samples were also tested by single radial hemolysis test. Seropositivity was only confirmed by both methods in one (0.13%; 95% CI: 0.00 to 0.38) sample of 2013 adult animal.

Apigenin suppresses influenza A virus-induced RIG-I activation and viral replication
Apigenin suppresses influenza A virus-induced RIG-I activation and viral replication

Abdomen and pelvis Organ Failure Induced by intraperitoneal Influenza A Virus Infection in Mice

In humans, respiratory infections with influenza A virus can be deadly, but it is unclear whether influenza A non-breathing can be equally deadly. Intraperitoneal Infection making organs of the abdomen and pelvis accessible to pathogens because peritoneal fluid circulation around the pelvis and abdomen.

We found that high doses of intraperitoneal infection in mice with influenza virus A and sclerosis resulted in structural damage in the pancreas, ovarian follicle disorders, and a large infiltration of immune cells in the uterus. Intraperitoneal infection also causes a strong upregulation of proinflammatory mediators, including IL-6, BLC, and MIG. In addition, low doses of intraperitoneal infection with the influenza strain is provided cross-protection against subsequent intraperitoneal or intranasal challenge with other strains of influenza.

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Our results suggest that low-dose, non-respiratory administration may provide a route for influenza vaccination. Furthermore, these results provide insight into the pathological role of influenza A virus in high-risk patients, including women and people with diabetes.

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