Hepatitis E virus infection activates signal regulator protein α 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 α (SIRP-α) plays an important role in negative regulation of innate immunity. In the present study, HEV infection significantly activated the expression of SIRP-α and down-regulated phosphorylation of IRF3, consequently resulted in suppression of type I interferon (IFN-β). In conclusion, HEV exploited SIRP-α to negative regulated IFN-β of the host innate immune system to promote viral infection. It suggested that interfering with the functions of SIRP-α should be considered as a potential therapeutic approach to the prevention and treatment of HEV infection.
Fen
F
Huang
Chenchen
C
Yang
Wenhai
W
Yu
Yanhong
Y
Bi
Feiyan
F
Long
Jue
J
Wang
Yunlong
Y
Li
Shenrong
S
Jing
D000943:Antigens, Differentiation / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D057809:HEK293 Cells; D016751:Hepatitis E / Q000188:drug therapy / Q000276:immunology*; D016752:Hepatitis E virus / Q000502:physiology*; D054884:Host-Pathogen Interactions; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate / Q000235:genetics; D050838:Interferon Regulatory Factor-3 / Q000235:genetics / Q000378:metabolism; D016899:Interferon-beta / Q000378:metabolism; D058990:Molecular Targeted Therapy; D010766:Phosphorylation / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D011971:Receptors, Immunologic / Q000235:genetics / Q000378:metabolism*; D014779:Virus Replication
D000943:Antigens, Differentiation; C494232:IRF3 protein, human; D050838:Interferon Regulatory Factor-3; D034741:RNA, Small Interfering; D011971:Receptors, Immunologic; C501920:SIRPA protein, human; D016899:Interferon-beta