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Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Microbiol 2020 ; 22 (5): e13150 Nephropedia Template TP
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Human microRNA-30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4 #MMPMID31876380
Lin X; Yu S; Ren P; Sun X; Jin M
Cell Microbiol 2020[May]; 22 (5): e13150 PMID31876380show ga
Influenza A virus (IAV) has evolved multiple mechanisms to compromise type I interferon (IFN) responses. The antiviral function of IFN is mainly exerted by activating the JAK/STAT signalling and subsequently inducing IFN-stimulated gene (ISG) production. However, the mechanism by which IAV combat the type I IFN signalling pathway is not fully elucidated. In this study, we explored the roles of human microRNAs modulated by IAV infection in type I IFN responses. We demonstrated that microRNA-30 (miR-30) family members were downregulated by IAV infection. Our data showed that the forced expression of miR-30 family members inhibited IAV proliferation, while miR-30 family member inhibitors promoted IAV proliferation. Mechanistically, we found that miR-30 family members targeted and reduced SOCS1 and SOCS3 expression, and thus relieved their inhibiting effects on IFN/JAK/STAT signalling pathway. In addition, miR-30 family members inhibited the expression of NEDD4, a negative regulator of IFITM3, which is important for host defence against influenza viruses. Our findings suggest that IAV utilises a novel strategy to restrain host type I IFN-mediated antiviral immune responses by decreasing the expression of miR-30 family members, and add a new way to understand the mechanism of immune escape caused by influenza viruses.
|A549 Cells[MESH]
|Down-Regulation[MESH]
|HeLa Cells[MESH]
|Host-Pathogen Interactions/immunology[MESH]
|Humans[MESH]
|Influenza A virus/*drug effects/genetics[MESH]
|Influenza, Human/*drug therapy[MESH]
|MicroRNAs/genetics/*pharmacology[MESH]
|Nuclear Proteins/genetics/*metabolism[MESH]
|RNA-Binding Proteins/genetics/*metabolism[MESH]
|Suppressor of Cytokine Signaling 1 Protein/genetics/*metabolism[MESH]