| Background: Type I interferon, including IFN-alpha and IFN-beta, is a kind of cytokine involved in antiviral defence. Nowadays, IFN-alpha has been applied in virologic diseases especially in viral hepatitis and is considered as one of the most important antiviral drugs. However, the therapy effect of IFN-alpha in patients with hepatitis B virus is only 20-40%, dueing to multiple causes such as various viral gene type, viral gene mutation. In the Interferon-virus system, the effectiveness of the IFN response has led to many viruses developing specific mechanisms to circumvent the IFN response, either by limiting IFN production or by blocking IFN actions. As the struggle between the virus and IFN lasting, the effect of viral countermeasure to IFN appears more and more significant, which benefits for virus to replicate efficiently in vivo. But researches about the countermeasure of HBV to IFN response are rare. By studying the mechanisms by which HBV circumvent the IFN response, we can understand more about HBV pathogenesis and unsuccess in the treatment of HBV infections. And even more, it may be possible to identify new and unsuspected insights into HBV therapy. Since either endogenous or exogenous type I interferon exerting its antiviral effect requires its binding to the specificreceptor on the target cell membrane, the type I receptor does an important role in interferon antiviral response. Deficiency of type I interferon, cellular expression level of the receptor on the target cell or the binding function between IFN and receptor will be relative to the extent of type I interferon's antiviral response.Objective: We investigated the difference in cellular expression of type I interferon receptor in the HBV-transfected HepG2.2.15 cell line and untransfected HepG2 cell line in order to find the affect of HBV on the expression of type I interferon receptor on target cell membrane. We tried to find some new explain for the difference of clinical interferon response which will benefit us to detect some new methods to increase the interferon response.Methods: Three relative cell lines were applied in this experiment: L02 cell line is the normal hepatic cell line; HepG2 cell line is the human hepatocellular carcinoma cell line; 2.2.15 cell line is HepG2 cell transfected HBV genome. FCM was used to investigate the expression level of type I IFN receptor beta subunit on the cellular surface or in cytoplasm, and the positive percent was used as parameter to statistics analyze. Western blot was used to study the level of alpha and beta subunits with the same protein loading and beta-actin was used as the internal control to measure the loading protein.Results: The positive percent of IFNAR beta subunit on HepG2 cell membrane was (79.8+5.37)%, and in cytoplasm was (83.55+7.28)%; while for 2.2.15 cell, the positive percent was (39.67+3.84)% and (49.00+6.08)%, respectively. Comparing the results to hepG2 cell group, expressions of beta subunit of IFNAR on 2.2.15 cell surface and in cytoplasm were much lower than on HepG2 cell and the difference was significant in statistics(p<0.01). The positive percent of IFNAR beta subunit on L02 cell membrane was (48.97+6.01)%, and in cytoplasm was (48.60+7.35)%; although the expression of IFNAR beta subunit was lowered significantly on L02 cell comparing with HepG2 cell, the difference between L02 and 2.2.15 was slight. Further study about expression of IFNAR byWestern blot, we detected the bands representing the alpha and beta subunit of IFNAR of 2.2.15 cell were much weaker than HepG2's. However, the difference between HepG2 and L02 cell was slight.Conclusion: Since the expression level of both subunits of type I interferon receptor on 2.2.15 cell was much lower than on HepG2 cell, it suggests HBV can down-regulate the expression of type I receptor.
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