HCV-Induced miR-21 Contributes to Evasion of Host Immune System by Targeting MyD88 and IRAK1
文献类型：期刊论文
| 作者 | Chen, Yanni2,3,4; Chen, Junbo2,3; Wang, Hui2,3; Shi, Jingjing2,3; Wu, Kailang1,2,3; Liu, Shi2,3; Liu, Yingle1,2,3; Wu, Jianguo1,2,3 |
| 刊名 | PLOS PATHOGENS
 |
| 出版日期 | 2013-04-01 |
| 卷号 | 9期号:4页码:20 |
| ISSN号 | 1553-7374 |
| DOI | 10.1371/journal.ppat.1003248 |
| 英文摘要 | Upon recognition of viral components by pattern recognition receptors, such as the toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like helicases, cells are activated to produce type I interferon (IFN) and proinflammatory cytokines. These pathways are tightly regulated by the host to prevent an inappropriate cellular response, but viruses can modulate these pathways to proliferate and spread. In this study, we revealed a novel mechanism in which hepatitis C virus (HCV) evades the immune surveillance system to proliferate by activating microRNA-21 (miR-21). We demonstrated that HCV infection upregulates miR-21, which in turn suppresses HCV-triggered type I IFN production, thus promoting HCV replication. Furthermore, we demonstrated that miR-21 targets two important factors in the TLR signaling pathway, myeloid differentiation factor 88 (MyD88) and interleukin-1 receptor-associated kinase 1 (IRAK1), which are involved in HCV-induced type I IFN production. HCV-mediated activation of miR-21 expression requires viral proteins and several signaling components. Moreover, we identified a transcription factor, activating protein-1 (AP-1), which is partly responsible for miR-21 induction in response to HCV infection through PKC epsilon/JNK/c-Jun and PKC alpha/ERK/c-Fos cascades. Taken together, our results indicate that miR-21 is upregulated during HCV infection and negatively regulates IFN-alpha signaling through MyD88 and IRAK1 and may be a potential therapeutic target for antiviral intervention. |
| 资助项目 | Major State Basic Research Development Program (973 Program)[2012CB518900] ; Major State Basic Research Development Program (973 Program)[2009CB522506] ; National Natural Science Foundation of China[31230005] ; National Natural Science Foundation of China[812111146] ; National Natural Science Foundation of China[81171525] ; National Mega Project on Major Infectious Disease Prevention[2012ZX10002006-003] ; National Mega Project on Major Infectious Disease Prevention[2012ZX10004-207] ; National Mega Project on Major Drug Development[2011ZX09401-302] |
| WOS研究方向 | Microbiology ; Parasitology ; Virology |
| 语种 | 英语 |
| WOS记录号 | WOS:000318072700008 |
| 出版者 | PUBLIC LIBRARY SCIENCE |
| 源URL | [http://202.127.146.157/handle/2RYDP1HH/3859]  |
| 专题 | 中国科学院武汉植物园 |
| 通讯作者 | Chen, Yanni |
| 作者单位 | 1.Wuhan Inst Biotechnol, Wuhan, Hubei, Peoples R China 2.Wuhan Univ, Zhongnan Hosp, Coll Life Sci, State Key Lab Virol, Wuhan 430072, Hubei, Peoples R China 3.Wuhan Univ, Zhongnan Hosp, Chinese French Liver Dis Res Inst, Wuhan 430072, Hubei, Peoples R China 4.Chinese Acad Sci, State Key Lab Virol, Wuhan Inst Virol, Wuhan, Hubei, Peoples R China |
| 推荐引用方式 GB/T 7714 | Chen, Yanni,Chen, Junbo,Wang, Hui,et al. HCV-Induced miR-21 Contributes to Evasion of Host Immune System by Targeting MyD88 and IRAK1[J]. PLOS PATHOGENS,2013,9(4):20. |
| APA | Chen, Yanni.,Chen, Junbo.,Wang, Hui.,Shi, Jingjing.,Wu, Kailang.,...&Wu, Jianguo.(2013).HCV-Induced miR-21 Contributes to Evasion of Host Immune System by Targeting MyD88 and IRAK1.PLOS PATHOGENS,9(4),20. |
| MLA | Chen, Yanni,et al."HCV-Induced miR-21 Contributes to Evasion of Host Immune System by Targeting MyD88 and IRAK1".PLOS PATHOGENS 9.4(2013):20. |
入库方式： OAI收割
来源：武汉植物园
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