Effects of Schlafen gene family on HBV replication
10.3760/cma.j.issn.0254-5101.2019.12.002
- VernacularTitle: Schlafen基因家族对HBV复制的影响
- Author:
Binli MAO
1
;
Xing ZHOU
;
Sidie PI
;
Yuan HU
Author Information
1. Key Laboratory of Molecular Biology on Infectious Disease, Ministry of Education, Chongqing Medical University, Chongqing 400016, China
- Publication Type:Journal Article
- Keywords:
SLFN;
IFN-α;
Hepatitis B virus;
Antivirus
- From:
Chinese Journal of Microbiology and Immunology
2019;39(12):892-897
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the regulatory effects of interferon-stimulated gene Schlafen (SLFN) on hepatitis B virus (HBV) replication.
Methods:Firstly, HepG2 cells were treated with IFN-α at different concentrations for 48 h or the same concentration for different periods of time. Expression of SLFN family genes was detected by quantitative real-time PCR (q-PCR). Secondly, the expression of SLFN gene family at mRNA level in HBV-infected tumor tissues and non-tumor tissues recorded in The Cancer Genome Atlas (TCGA) database was compared using t test. Furthermore, changes in the HBV DNA levels after the interference of small interfering RNA (siRNA)-mediated knockdown and overexpression of SLFN5 and SLFN11 genes were analyzed by q-PCR, Western blot and Southern blot.
Results:Among the SLFN gene family, only SLFN5 expression was induced by IFN-α in a concentration-dependent manner. TCGA database analysis showed that the expression of both SLFN5 and SLFN11 in HBV-infected tumor tissues and non-tumor tissues was significantly different. In HepG2 cells, knocking down the expression of SLFN5 had no obvious effect on the levels of intracellular HBV DNA. It was observed that the level of intracellular HBV DNA increased 1.79 folds in Huh7 cells after knockdown of SLFN11 expression, while no significant change in HBc protein was detected. Conversely, overexpression of SLFN11 induced a 34.67% decrease in intracellular HBV DNA in HepG2 cells.
Conclusions:In HepG2 cells, SLFN5 expression was induced by IFN-α, but had no effect on HBV replication. However, SLFN11 could inhibit the HBV DNA replication in nucleocapsid.
