ACTA VETERINARIA ET ZOOTECHNICA SINICA ›› 2016, Vol. 47 ›› Issue (10): 2108-2114.doi: 10.11843/j.issn.0366-6964.2016.10.020

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Activation of Cold-inducible RNA-binding Protein by H1N1 Influenza Virus Contributes to Viral Replication Via Activating NF-κB Pathway

NIE Pei-ting,TANG Cheng,YUE Hua*   

  1. (College of Life Science and Technology,Southwest University for Nationalities,Chengdu 610041,China)
  • Received:2016-05-06 Online:2016-10-23 Published:2016-10-23

Abstract:

 The cold-inducible RNA-binding protein (CIRP) is an upstream regulator of the NF-κB and ERK pathways,which are essential for the replication of the influenza virus and the initial immune response.In order to investigate the effect of CIRP on the replication of H1N1 influenza A virus and its possible molecular mechanism,in this study,CIRP overexpression BHK-21 (Cirp+BHK-21) cells were constructed,and the phosphorylation levels of NF-κB and ERK in Cirp+BHK-21 cells were detected by Western blot to confirm the effect of CIRP on regulation of NF-κB and ERK1/2;Real-time RT-PCR was used to detect the dynamic changes of virus load in Cirp+BHK-21 and control cells after infected with influenza A virus,the method was also used to detect the dynamic changes of virus load in Cirp+BHK-21 cells which were blocked by the NF-κB inhibitor PDTC.The results of Western blot exhibited that overexpressed CIRP could significantly increase the expression of phosphorylation level of NF-κB (P<0.05),but had no significant effect on the phosphorylation level of ERK.The results of quantitative detection of virus showed that overexpressed CIRP could significantly enhance the proliferation of influenza A virus,the virus load in the Cirp+BHK-21 cells were 111%,103%,167% and 235% (P<0.05) at 3,9,15 and 21 h PI,respectively,compared to the control group;Blocking the NF-κB was significantly decreased the virus load in the Cirp+BHK-21,and the virus load in treatment group were 98%,42%,19% (P<0.05),7% (P<0.05) at 3,9,15 and 21 h PI,respectively,compared to the unblock group.Therefore,this study confirmed that overexpressed CIRP could enhance the proliferation of influenza A virus via activation of NF-κB pathway.

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