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.

Objective To investigate the regulatory role of host restriction factor Moloney leukemia virus 10 (MOV10) protein in HBV replication. Methods Firstly, a HBV replication-expression plasmid was transfected into Huh7 cells to investigate the effect of HBV replication on MOV10 expression. Secondly, HBV DNA was extracted and measured by quantitative PCR ( qPCR) after knocking down the expression of endogenous MOV10 or enhancing the expression of exogenous MOV10. Furthermore, MOV10 conserved do-mainⅡenzyme active mutants (D645A, E646Q and G648A) were constructed and analyzed regarding their antiviral activities. The HBV replication plasmid and MOV10 expression plasmid were co-transfected into hu-man renal epithelial cells (HEK293) to investigate whether MOV10 could bind to HBV mRNA using RNA binding protein immunoprecipitation ( RIP) . Results The expression of MOV10 was increased after trans-fection of HBV replication plasmid into Huh7 cells. After knocking down the expression of endogenous MOV10 by siRNA in Huh7 cells, HBV replication was increased about 1. 5 times compared with control group, while the viral DNA level was significantly decreased in Huh7 cells that overexpressed MOV10. MOV10 domain Ⅱ mutants also significantly inhibited HBV replication. MOV10 could bind to 3. 5 kb HBV RNA. Conclusion In liver cancer cells, the expression of the host restriction factor MOV10 was associated with HBV replication. Its inhibitory effect against HBV replication was independent of its helicase activity, but might be associated with its binding activity with 3. 5kb HBV RNA.