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Virologica Sinica, 32 (4) : 261, 2017
Research Article
Influenza A virus-induced downregulation of miR-26a contributes to reduced IFNα/β production
1. The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Collaborative Innovation Center for Cardiovascular Disorders, Beijing Institute of Heart, Lung & Blood Vessel Diseases
Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China
2. CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
3. Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, China
4. Beijing Municipal Center for Food Safety Monitoring and Risk Assessment, Beijing 100053, China
 Correspondence: gao_shijuan@163.com;hwenl@mail.sysu.edu.cn
(3526.25KB)  (266.68KB)  
Abstract
Innate immunity provides immediate defense against viral infection.Influenza A virus (IAV) is able to get past the first line of defense.Elucidation of the molecular interaction between influenza factors and the newly recognized host players in the innate response might help in our understanding of the root causes of virulence and pathogenicity of IAV.In this study,we show that expression of miR-26a leads to a significant inhibition of IAV replication.miR-26a does not directly target IAV genome.Instead,miR-26a activates the type I interferon (IFN) signaling pathway and promotes the production of IFN-stimulated genes,thus suppressing viral replication.Furthermore, ubiquitin-specific protease 3(USP3),a negative regulator of type I IFN pathway,is targeted by miR- 26a upon IAV challenge.However,miR-26a is significantly downregulated during IAV infection. Thus,downregulation of miR-26a is a new strategy evolved by IAV to counteract cellular antiviral responses.Our findings indicate that delivery of miR-26a may be a potential strategy for anti-IAV therapies.
Received: 22 Apr 2017  Accepted: 22 Apr 2017  Published online: 30 Jun 2017
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