ISGF3, a critical factor of the IFN-alpha pathway in the antiviral action of HBV.
- Author:
Quan ZHANG
1
;
Lai WEI
;
Yan WANG
Author Information
- Publication Type:Journal Article
- MeSH: Antiviral Agents; pharmacology; Blotting, Western; Cell Line, Tumor; DNA, Viral; genetics; isolation & purification; Gene Expression Regulation, Neoplastic; drug effects; Hepatitis B virus; drug effects; genetics; growth & development; Humans; Interferon-Stimulated Gene Factor 3; genetics; metabolism; Interferon-Stimulated Gene Factor 3, gamma Subunit; genetics; metabolism; Interferon-alpha; pharmacology; Polymerase Chain Reaction; RNA, Messenger; genetics; metabolism; Reverse Transcriptase Polymerase Chain Reaction; STAT1 Transcription Factor; genetics; metabolism; STAT2 Transcription Factor; genetics; metabolism; Signal Transduction
- From: Chinese Journal of Experimental and Clinical Virology 2005;19(2):110-113
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the mechanism of signal transduction in anti-HBV action of IFN-alpha.
METHODSThe HBV DNA in HepG 2.2.15 cell line supernatant with/without IFNalpha-2b were monitored by fluorescence real-time quantitive PCR. STAT1, STAT2, ISGF3-gamma, PKR, 2'5'-OAS mRNA levels from HepG 2 and HepG 2.2.15 cell lines that were treated with/without IFNalpha-2b at different times were detected by semi-quantitive RT-PCR. And the ISGF3-gamma protein was detected by Western blot. Then, these items were detected again after inhibiting the JAK-STAT pathway with genistein.
RESULTSThe HBV DNA in 2215 supernatant that were treated with IFNalpha-2b for 8 hours decreased 0.72 log 10 copies/ml. But the basal levels of DNA in cells pretreated with genistein? followed by IFNalpha-2b did not decrease. The STAT1, STAT2, ISGF3-gamma, 2'5'-OAS, PKR mRNA levels were upregulated by IFNalpha-2b. The same phenomena were observed with STAT1, STAT2, ISGF3-gamma mRNA when pretreated with genistein then treated with IFNalpha-2b, but the levels of 2'5'-OAS, PKR mRNA were decreased in this situation. The expression of the protein of ISGF3-gamma was also augmented by IFNalpha-2b, and was blocked by genistein.
CONCLUSIONThe JAK-STAT pathway seems to be a critical pathway in IFNalpha-2b action against HBV? and ISGF3 is most probably a key factor of the route.
