ABSTRACT
When hepatitis B virus (HBV) invades the human body, innate immunity acts the earliest and plays an important role. When an adult is infected with HBV, HBV can often be eliminated spontaneously. However, if HBV infection occurs right after birth or when the patient is young, the disease tends to become chronic and affect the whole life. In the incipient stage of HBV infection, innate immune response plays an important role in inhibiting viral replication, and the prognosis of HBV infection depends on the combined effect of host and virus. This article briefly introduces the research advances in the cells, cytokines, and signaling pathways that play important roles in the host's innate immunity against HBV and their mechanisms of action, and points out their potential values in clinical treatment.
ABSTRACT
Objective To investigate the characteristics of HBV replication in HepG2.2. 15 cells treated with LAM alone or sequentially treated with LAM and IFN-α, and to further explore the different suppressive effect on HBV replication by LAM and IFN-α in vitro. Methods Untreated HepG2. 2. 15 cells were used as control group, HepG2. 2. 15 cells treated with 1 000 IU/ml of IFN-α alone for 10 d were served as IFN-α group. The HepG2.2. 15 cells treated with 0.2,1,5,20,100 μmol/L of LAM were used as LAM groups. HepG2. 2. 15 cells treated with 0. 04,0. 2,5,25,125,200 μmol/L of LAM for 7 d, then combined with 1 000 IU/ml of IFN-α for another 3 d. Afterwards, the cells were treated with 1 000 IU/ml of IFN-α only for another 10 d. These cells were served as LAM/IFN-α sequential treatment group. The ELISA was used for analyzing the secreted HBV antigens, while the Dot blot, Southern blot were applied for analyzing the extracellular HBV DNA and intracellular HBV replicative intermediate DNA in HepG2. 2. 15 cells of different treatment groups. Results The secreted HBsAg in the LAM group were 1. 77 ± 0. 22, 1.65 ±0.25, 1.95 ±0. 19, 1.34 ±0. 11, 1.07 ±0.05, respectively, and the secretion of HBeAg were 1.41 ±0. 13, 1.37 ± 0. 09, 1.63 ± 0. 07, 1.26 ± 0. 12, 1.05 ± 0. 09. The secreted HBsAg and HBeAg in control group were 3. 34 ± 0. 15 and 3.33 ± 0. 05. Statistical analysis showed that HBsAg and HBeAg secretion in the LAM group were significantly reduced by treatment with LAM. The t values of HBsAg were 10. 21,10.04, 9.94, 18.62, 24.86, and the t values of HBeAg were 23.87, 32.97, 34.22, 27.57, 38.35,respectively, all P values were ＜ 0.05. Dot blot, Northern blot hybridization analysis indicated that the extracellular HBV DNA and intracellular HBV replicative intermediate DNA could not be detected in the LAM group after cells treated by LAM for 10 days. When LAM was replaced with treatment of 1 000 IU/ml of IFN-α alone, it could not suppress the HBV replication effectively. Moreover, the intracellular HBV replicative intermediate DNA still existed in almost all groups, accompanied with the recovered expression of HBV antigens as well as extracellular HBV DNA, which suggested that the HBV particles restored replication again and secreted extracellular in HepG2. 2. 15 cells, although the sequential treatment lasted for 10 days.Conclusion The effect of viral suppression by LAM and IFN-α in vitro were different, which attributed to the different HBV replicative characteristcs in HepG2. 2. 15 cells.
ABSTRACT
Previous studies have shown that expression of the interferon-sensitive gene (ISG)I5 protease UBP43 is increased in the liver biopsy specimens of patients who do not respond to interferon (IFN)-α therapy. We hypothesized that UBP43 might hinder the ability of IFN to inhibit HBV replication. In this study, we investigated whether vector-based siRNA promoted by Hi (psiUBP43) could enhance IFN inhibiting HBV replication in cell culture. UBP43 was specifically silenced using shRNA. In HepG2.2.15 cells, the HBeAg and HBV DNA levels were significantly reduced by IFN after transfection of shRNA, imphicated that vector-based siRNA promoted by HI (psiUBP43) could enhance IFN inhibiting HBV replication in cell culture. These data suggest that UBP43 modulates the anti-HBV type I IFN response, and is a possible therapeutic target for the treatment of HBV infection.
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Objective To establish the ELISA method by using synthetic peptide for detection of IgM antibodies to human cytomegalovirus(HCMV).Methods According to HCMV PP150 sequence of amino acid and nucleotide,the peptide sequence was decided by computer with some program of software of protein.The ELISA method using synthetic peptide as antigen was developed and was applied to detected anti-HCMV IgM in sera of normal pregnant woman and habitual abortion woman.The HCMV DNA were detected by polymerase chain reaction(PCR).Results The positive rates of anti-HCMV IgM in different populations were as follows:9 17%(11/120) in normal pregnant woman,37 5%(24/64) in habitual abortion woman.The ELISA method have good speciality.The positive rate of HCMV DNA was significantly related to that of anti-HCMV IgM(P
ABSTRACT
Objective To detect the expression of interferon-?(IFN-?) and interleukin 12(IL-12) in peripheral blood mononuclear cells(PBMCs) of patients with chronic hepatitis B and analyze cellular immune status of the patients with chronic hepatitis B virus(HBV) infection.Methods The PBMCs of patients with chronic HBV infection were cultured,then the antiviral biological activity of PBMCs stimulated with high concentration of PolyIC in the culture supernatants was detected by viral protection assay.IL-12 mRNA in PBMCs from the patients with chronic hepatitis B was measured by reverse transcription polymerase chain reaction(RT-PCR).Results The obtained data indicated that lower titer of IFN-?from PolyIC-induced PBMCs existed in patients infected by chronic HBV.Enhanced IFN-?activity from PBMCs stimulated by PolyIC was found in the responder(n=4) who were treated with IFN-?2b.However,continuously lower activity of IFN-?from PBMCs presented in non-responder(n=12) during IFN-?2b therapy.The expressions of IL-12 mRNA in PBMCs from both responder and non-responder were significantly higher than those of normal control group(n=10) before treatment with IFN-?2b(P