tetano
Editor, Senior Moderator
Cell Microbiol. 2019 Dec 26:e13150. doi: 10.1111/cmi.13150. [Epub ahead of print] [h=1]Human microRNA-30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4.[/h]
Lin X[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Yu S[SUP]1,[/SUP][SUP]2[/SUP], Ren P[SUP]1,[/SUP][SUP]2[/SUP], Sun X[SUP]1,[/SUP][SUP]2[/SUP], Jin M[SUP]1,[/SUP][SUP]2,[/SUP][SUP]4,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h] 1 State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China. 2 Department of Preventive Veterinary Medicine, College of Animal Medicine, Huazhong Agricultural University, Wuhan, China. 3 Department of Biotechnology, College of Life Science and Technology, Huazhong Agricultural University, Wuhan, China. 4 Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China. 5 The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, China.
[h=3]Abstract[/h] 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.
? 2019 John Wiley & Sons Ltd.
[h=4]KEYWORDS:[/h] NEDD4; SOCS1; SOCS3; influenza virus; microRNA-30
PMID: 31876380 DOI: 10.1111/cmi.13150
Lin X[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Yu S[SUP]1,[/SUP][SUP]2[/SUP], Ren P[SUP]1,[/SUP][SUP]2[/SUP], Sun X[SUP]1,[/SUP][SUP]2[/SUP], Jin M[SUP]1,[/SUP][SUP]2,[/SUP][SUP]4,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h] 1 State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China. 2 Department of Preventive Veterinary Medicine, College of Animal Medicine, Huazhong Agricultural University, Wuhan, China. 3 Department of Biotechnology, College of Life Science and Technology, Huazhong Agricultural University, Wuhan, China. 4 Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China. 5 The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, China.
[h=3]Abstract[/h] 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.
? 2019 John Wiley & Sons Ltd.
[h=4]KEYWORDS:[/h] NEDD4; SOCS1; SOCS3; influenza virus; microRNA-30
PMID: 31876380 DOI: 10.1111/cmi.13150