Nucleoside analogues are currently the main drug therapy against HBV infection. However, this type of therapy can cause gene mutations in HBV that result in drug resistance. The types of mutations caused by nucleoside analogues and the molecular mechanism of in vitro drug-resistance were reveiwed.

Hantavirus is the main cause of hemorrhagic fever with renal syndrome (HFRS). It is an acute infectious diseases characterized by fever, hemorrhage, nephritis or thrombocytopenia, and hantavirus pulmonary syndrome(HPS). The main clinical manifestations are fever, hemorrhagic lesion, acute respiratory distress and capillary leakeage syndrome. These are four different serotypes of the hantavirus species: Hantan virus(HTNV),Seoul virus(SEOV),Dobrava/Belgrade virus(DOBV),and Puumala virus(PUUV). They are known to cause HFRS, while Sin Nombre virus(SNV) causes HPS. In China, these are two serotypes of hantavirus: HTNV and SEOV found. The severity of infection depends on the viral serotype. To find a safe, rapid and specific serotyping diagnosis of the causative virus is important. The results not only can be beneficial for rodent control, but also for prevention and therapy. The current research of Hantavirus nucleocapsid protein used as serotyping antigen are summarized.

Current therapies for chronic hepatitis caused by hepatitis B virus (HBV) are limited. RNA interference (RNAi) may constitute a new therapeutic strategy for various hepatitis virus infections. In this review we present the advances in inhibition of HBV by RNAi, the unresolved questions and therapeutic potential of RNAi.

Objective To detect circulating CD4 + CD25 + regulatory T cells (Treg) and Toll-like receptor(TLR)2 and TLR4 expression on the peripheral blood mononuclear cells (PBMCs) of patients with HBV-related liver cirrhosis (LC), and to explore the correlation between them. Methods PBMCs isolated from 30 LC patients, 21 chronic hepatitis B (CHB) patients and 16 normal controls(NC) were stained with fluorescent labeling anti-TLR2-PE, anti-TLR4-APC, anti-CD14-FITC monoclonal antibodies and anti-CD4-PerCP, anti-CD25-FITC, anti-CD127-PE. Samples were detected by flow cytometry. Statistic analysis be-tween groups was performed by Kruskal-Wallis H test. Spearman rank correlation was used to analyze the correlation of Treg and TLR2, TLR4. Results The expression of TLR2 and TLR4 were significantly up-reg-ulated in patients with LC than those in the controls (TLR2 : 200.3 ± 96.8 vs 94.1 ± 17.6, P < 0.05 ; TLR4:32.1 ±7.2 vs 17.8 ±3.9, P<0.05). The expression of TLR4 was significantly increased in pa-tients with LC than those in patients with CHB (TLR4 : 32. 1 ± 7.2 vs 25.2 ± 8.3, P < 0.05), but there were no differences of TLR2 expression between LC and CHB(200.3 ± 96.8 vs 214.0 ± 72.6, P > 0.05). Treg/CD4+ T cells were 5.07% ±1.43%, 5.88% ±1.66%, 4.21% ±1.24% in patients with LC, CHB and NC, respectively. Treg/CD4+ T cells were significantly increased in patients with CHB than those in pa-tients with NC(P<0. 05) and LC(P <0.05), but there were no differences between LC and NC(P > 0.05). TLR4 expression and Treg were positive correlation (r = 0. 469, P = 0. 032) and TLB2 expression were negative correlation in patients with LC (r = -0.428, P = 0.021). Conclusion The expression of TLR2 and TLR4 were up-regulated on PBMCs in patients with LC. It seems to be expression of TLR2 and TLR4 in-volved in the pathogenesis of LC.

The study on bioartificial liver support system was widely accepted in recent years. It's mainly containing material-hepatocytes. This summary is concerning about the research and application of hepatocytes in this field.

Objective:To observe the therapeutic effects of plasma exchange in severe hepatitis. Methods:53 cases served as treatment group and 49 cases as control group. Both groups were similar in basic medical treatment, and an additional treatment of plasma exchange was carried in the treatment group. 186 times of plasmas exchange were performed in the treatment group, to observe and compare the changes in patients of the 2 groups in symptoms、liver functions and survival rates. Results:The clinical symptoms of patients in the treatment group were obviously improved, the liver functions were also obviously improved in the treatment group as compared with the control group, and the survival rate of treatment group was higher than that of control group(73.58% vs 46.94%, P

Objective:To study the different effect of fused gene IL-2/Fc administrated at different time on immune responses induced by HBV preS_2S genetic vaccine.Methods:BALB/c mice were immunized with purified recombinant plasmids at 0, 2, 4 weeks. Two groups were designed. One group were injected with pcDNA3.1S_2S at first, then pcDNA3.1IL-2/Fc was administrated after three days. While the other group were injected two plasmids at the same time. We compared the immune responses through detecting the anti-HBs titers, CTL cytotoxicity level, proliferation of lymphocytes and cytokines levels secreted by cultural splenocytes.Results:The data demonstrated that the humoral and cellular immune responses induced by pcDNA3.1IL-2/Fc as adjuvant and administrated after HBV preS_2S DNA vaccine 3 days mice were dominant higher than other groups.Conclusion:Genetic adjuvant administrated after Ag priming can enhance its effect.

Objective To observe the nuclear translocation of transcription factor NF-κB and IRF-3 in TLR4 silenced EVC304 cells infected by HTNV and to provide new information for anti-HTNV innate immunity and its signal transduction. Methods TLR4~- cells and TLR4~+ cells were infected by HTNV 76-118, respectively. The cells stimulated by LPS were selected as positive control groups, and the cells without stimulation were selected as negative control groups. After 6 hours, indirect immunofluorescence assay(IFA) was used to detect the nuclear translocation of NF-κB and IRF-3. Results The transcription factor NF-κB and IRF-3 transfered into nuclear 6 hours after stimulated by HTNV 76-118. Conclusion TLR4 may mediate the nuclear translocation of transcription factor NF-κB and IRF-3 in HTNV infected human umbilical vein endothelial cells.

Objective To develop a reverse genetics system for Hantaan virus (HTNV) 84FLi strain by using RNA polymerase [ (pol Ⅰ)-mediated transcription. Methods Complementary DNA (cDNA) containing the coding sequence for chloramphenicol acetyhransferase (CAT) was inserted into the 5'-and 3'-terminal untranslated regions of HTNV 84FLi L segment. These chimeric cDNAs (pol Ⅰ expression cassette) were cloned into plasmids and between the human pol Ⅰ promoter and terminator to generate sense and anti-sense RNA pol Ⅰ transcription reporter plasmids. The reporter plasmids were transfeeted into 293T cells or the 1:1 combination of 293T and HTNV infected Vero cells. These cells were cotransfected with expression plasmids encoding Ⅰ. (RNA dependent RNA polymerase) and N (nucleoprotein) viral proteins, Cells were harvested 48 h post-transfection and the CAT activity was detected. The 293T cells were infected with the supernatant to explore the passage ability of CAT activity. ResultsThe reporter plasmids pLvRNA-CAT and pLcRNA-CAT were constructed successfully. CAT activity was detected in transfected cells and could also be serially passaged in the rescued virus minigenomes. Conclusion The RNA polymerase ]-driven reverse genetics system successfully rescues HTNV 84FLi minigenomes.

Acute liver failure (ALF) is a syndrome characterized by rapid onset, rapid progression, and poor prognosis. Although much progress has been achieved in the etiology and pathogenesis of ALF and emergency liver transplantation and comprehensive treatment have significantly increased the treatment success rate, there are still many difficult issues in clinical practice. This article reviews the research advances in the classification, etiology, main clinical types, prognostic scoring system, and treatment of ALF in recent years.