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Hepatitis E virus infection activates signal regulator protein [alpha] to down-regulate type I interferon
Hepatitis E virus (HEV) is a major cause of enterically transmitted acute hepatitis worldwide. However, the mechanism of HEV replication is unclear. Type I interferon is the first defense line of host against viral infection. Signal regulator protein [alpha] (SIRP-[alpha]) plays an important role in...
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Published in: | Immunologic research 2016-02, Vol.64 (1), p.115 |
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creator | Huang, Fen Yang, Chenchen Yu, Wenhai Bi, Yanhong Long, Feiyan Wang, Jue Li, Yunlong Jing, Shenrong |
description | Hepatitis E virus (HEV) is a major cause of enterically transmitted acute hepatitis worldwide. However, the mechanism of HEV replication is unclear. Type I interferon is the first defense line of host against viral infection. Signal regulator protein [alpha] (SIRP-[alpha]) plays an important role in negative regulation of innate immunity. In the present study, HEV infection significantly activated the expression of SIRP-[alpha] and down-regulated phosphorylation of IRF3, consequently resulted in suppression of type I interferon (IFN-[beta]). In conclusion, HEV exploited SIRP-[alpha] to negative regulated IFN-[beta] of the host innate immune system to promote viral infection. It suggested that interfering with the functions of SIRP-[alpha] should be considered as a potential therapeutic approach to the prevention and treatment of HEV infection. |
doi_str_mv | 10.1007/s12026-015-8729-y |
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title | Hepatitis E virus infection activates signal regulator protein [alpha] to down-regulate type I interferon |
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