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Hepatitis B virus core protein interacts with CD59 to promote complement‐mediated liver inflammation during chronic hepatitis B virus infection
Author(s) -
Liu Dong,
Ni Bing,
Wang Li,
Zhang Mengjun,
Liu Wei,
Wu Yuzhang
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.08.044
Subject(s) - cd59 , hepatitis b virus , flow cytometry , virus , hepatocyte , virology , biology , complement system , immune system , microbiology and biotechnology , chemistry , immunology , in vitro , biochemistry
The inflammatory response mediated by the immune system is the major cause of hepatitis B virus (HBV)‐associated liver injury. Here, we identified CD59, as a novel HBc‐interacting protein in hepatocytes by tandem affinity purification (TAP) screening. The expression of CD59 was markedly down‐regulated in HBc‐transfected HepG2 or HepG2.215 cells, which resulted in an upshift of hepatocyte sensitivity to membrane attack complex (MAC)‐induced cell lysis. These results were consistent with the accumulation of MACs in the liver of HBV‐infected patients. Additional analyses using laser confocal microscopy, quantitative PCR and flow cytometry revealed that CD59 was specifically translocated to the nucleus upon binding to HBc, which induced the down‐regulation of CD59 on both the mRNA and protein levels.