机构：[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临床科室心脏内科中心首都医科大学附属安贞医院[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其他部门华南肿瘤学国家重点实验室中山大学肿瘤防治中心[4]Beijing Municipal Center for Food Safety Monitoring and Risk Assessment, Beijing 100053, China
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.
基金：
National Basic Research Program of China (973 Program) [2012CB518900]; Beijing Natural Science Foundation [7122109]
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2017]版：
无
最新[2023]版：
大类|3 区医学
小类|3 区病毒学
第一作者：
第一作者机构：[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
共同第一作者：
通讯作者：
通讯机构：[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
推荐引用方式(GB/T 7714)：
Gao Shijuan,Li Jiandong,Song Liping,et al.Influenza A virus-induced downregulation of miR-26a contributes to reduced IFN alpha/beta production[J].VIROLOGICA SINICA.2017,32(4):261-270.doi:10.1007/s12250-017-4004-9.
APA：
Gao, Shijuan,Li, Jiandong,Song, Liping,Wu, Jiaoxiang&Huang, Wenlin.(2017).Influenza A virus-induced downregulation of miR-26a contributes to reduced IFN alpha/beta production.VIROLOGICA SINICA,32,(4)
MLA：
Gao, Shijuan,et al."Influenza A virus-induced downregulation of miR-26a contributes to reduced IFN alpha/beta production".VIROLOGICA SINICA 32..4(2017):261-270
