BACKGROUND & AIMS:Coronavirus disease 2019 (COVID-19) is a major global health threat. We aimed to describe the characteristics of liver function in patients with SARS-CoV-2 and chronic hepatitis B virus (HBV) coinfection.METHODS:We enrolled all adult patients with SARS-CoV-2 and chronic HBV coinfection admitted to Tongji Hospital from February 1 to February 29, 2020. Data of demographic, clinical characteristics, laboratory tests, treatments, and clinical outcomes were collected. The characteristics of liver function and its association with the severity and prognosis of disease were described.RESULTS:Of the 105 patients with SARS-CoV-2 and chronic HBV coinfection, elevated levels of liver test were observed in several patients at admission, including elevated levels of alanine aminotransferase (22, 20.95%), aspartate aminotransferase (29, 27.62%), total bilirubin (7, 6.67%), gamma-glutamyl transferase (7, 6.67%), and alkaline phosphatase (1, 0.95%). The levels of the indicators mentioned above increased substantially during hospitalization (all P < .05). Fourteen (13.33%) patients developed liver injury. Most of them (10, 71.43%) recovered after 8 (range 6-21) days. Notably the other, 4 (28.57%) patients rapidly progressed to acute-on-chronic liver failure. The proportion of severe COVID-19 was higher in patients with liver injury (P = .042). Complications including acute-on-chronic liver failure, acute cardiac injury and shock happened more frequently in patients with liver injury (all P < .05). The mortality was higher in individuals with liver injury (28.57% vs 3.30%, P = .004).CONCLUSION:Liver injury in patients with SARS-CoV-2 and chronic HBV coinfection was associated with severity and poor prognosis of disease. During the treatment of COVID-19 in chronic HBV-infected patients, liver function should be taken seriously and evaluated frequently.

HBV pol plays a critical role in the replication of hepatitis B virus (HBV). Previous studies conducted on HBV pol have produced limited evidence on HBV pol expression due to the lack of effective detection methods. The present study used the HBV pol (159-406 aa) protein as a target to screen for specific monoclonal antibodies that recognize HBV pol and subsequently evaluate their diagnostic and therapeutic value. Four antibodies (P3, P5, P12, P20) against HBV pol were obtained. Among them, the P20 antibody indicated optimal binding with HBV pol as demonstrated by Western blotting (WB) in a cell model transfected with the HBV genome. We also expressed P5 and P12 antibodies in mouse liver cells by transfection and the results indicated significant antiviral effects caused by these two antibodies especially P12. In summary, the present study established an antibody which was denoted P20. This antibody can be used to detect HBV pol expression by four HBV genomes via WB analysis. In addition, the antibody denoted P12 could exert antiviral effects via intracellular expression, which may provide a promising approach for the treatment of chronic hepatitis B.

In early 2020, the outbreak of new coronavirus pneumonia broke out globally, and the assessment criteria for organ transplant donor infections also brought new changes. Under the situation of the new crown epidemic, it is necessary to update the infection assessment criteria for organ transplantation with regard to donor quality. The infectious pathogen spectrum of the absolute contraindications of donor organ donation has been updated, and the procedures for evaluating donor quality infections have changed accordingly. This review analyzes the infections from the donors by classification, and summarizes the treatment measures taken by the donors infected by different pathogens, and summarizes the evaluation standards and evaluation procedures of the donors' infection quality. © 2021, Editorial Board of Medical Journal of Wuhan University. All right reserved.

目的 探讨miR-203对酒精性肝病(ALD)大鼠肝损伤的保护作用及其作用机制.方法 将60只SD大鼠随机分为ALD组(A组)、NC-miRNA/ALD组(B组)和miR-203/ALD组(C组).将慢病毒质粒经尾静脉注射感染大鼠,并采用酒精饮料喂养法建立ALD模型,采用Realtime PCR法检测大鼠肝组织miR-203水平,常规行病理学检查,评估大鼠肝组织损伤情况.使用市售试剂盒检测大鼠肝组织匀浆超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和丙二醛(MDA)水平,采用Western Blot法检测肝组织IL-1β3和NF-κB蛋白表达.结果 在建模8 w末,C组大鼠肝组织miR-203水平为(2.8±0.1),显著高于B组[(1.3±0.5),P＜0.05];C组动物血清AST、ALT和TBIL水平分别为(89.5±7.9) U/L、(38.5±10.1) U/L和(27.8±5.1) μmol/L,显著低于B组[(162.8±16.5)U/L、(69.6±7.5) U/L和(54.9±7.8) μmol/L,P＜0.05];C组肝组织匀浆SOD和CAT水平分别为(57.6±11.4) U/mg和(54.6±9.9) U/mg,显著高于B组[(41.6±7.6) U/mg和(45.7±6.0) U/mg,P＜0.05],而MDA水平为(2.8±0.1) nmol/g,显著低于B组[(5.0±0.2)nmol/g,P＜0.05];Western Blot检测结果表明,C组肝组织IL-1β蛋白和NF-κB表达分别为(0.7±0.2)和(0.3±0.1),显著低于B组[(1.2±0.3)和(1.0±0.2),P＜0.05].结论 miR-203过表达对ALD大鼠肝损伤起到了保护作用,其可能的机制是增强了抗氧化和抗炎作用.

目的 评价比阿培南治疗慢性肝病合并急性细菌性感染的有效性和安全性.方法 采用多中心回顾性研究,820例慢性肝病合并急性细菌性感染患者,给予阿培南300 mg+0.9％氯化钠注射液100 mL静脉滴注,滴注时间30～180 min,q8 h或q6 h,治疗时间≥3 d,比阿培南一般疗程7～14 d.结果 比阿培南有效率75.73％.痊愈率、显效率、进步率、无效率及死亡率分别为22.45％,41.95％,23.22％,10.37％和2.01％.细菌清除率和假定清除率分别为42.86％和47.96％.药物不良反应发生率1.10％.结论 比阿培南治疗慢性肝病合并急性细菌性感染安全、有效.

目的:探讨基因1型戊型肝炎病毒(HEV)开放读码框3(ORF3)对人外周血来源的树突状细胞(DC)成熟和活化功能的影响.方法:抽取健康志愿者的外周血分离单个核细胞,经体外培养、诱导为DC.然后分别用含有ORF3的慢病毒载体以及空载载体感染DC 48h,流式细胞仪检测ORF3组、空载组和空白组细胞表面CD80、CD83、CD86的表达,ELISA法检测DC上清中IFN-β、IL-4、IL-10和IL-12的分泌.之后再加入TNF-α进一步刺激DC成熟,流式细胞仪检测各组细胞CD80、CD83、CD86以及IFN-β、IL-4、IL-10、IL-12的表达.最后将DC与T淋巴细胞共培养,CCK8法检测T淋巴细胞增殖.结果:含有ORF3组的DC与空载组相比,加入TNF前后,其细胞表面CD8o、CD83、CD86以及细胞上清中IFN-β、IL-4、IL-10和IL-12的表达都明显较低(P＜0.05).ORF3组与空载组相比其刺激T细胞增殖的能力也较弱(P＜0.05).结论:基因1型HEV ORF3可以抑制人外周血来源DC的成熟,抑制其分泌IFN-β、IL-4、IL-10和IL-12等细胞因子,抑制DC对T淋巴细胞的增殖刺激作用,从而削弱机体对HEV的免疫反应,实现免疫逃逸,可能是导致戊型肝炎慢性化的原因之一.

AIM:To assess the effects of hepatitis E virus (HEV) on the production of type I interferons (IFNs) and determine the underlying mechanisms.METHODS:We measured the production of interferon (IFN)-alpha and -beta (-α/β) in genotype 3 HEV-infected C3A cells at different time points (0, 8, 12, 24, 48, 72 and 120 h) by enzyme-linked immunosorbent assay (ELISA). The expression levels of IFN-stimulated gene (ISG)15 in HEV-infected C3A cells at different time points were tested by western blotting. The plasmid-expressing open reading frame 3 (ORF3) or control plasmids (green fluorescent protein-expressing) were transfected into C3A cells, and the levels of IFN-α/β and ISG15 were evaluated, respectively. Furthermore, the plasmid-expressing ISG15 or small interfering RNA-inhibiting ISG15 was transfected into infected C3A cells. Then, the production of IFN-α/β was also measured by ELISA.RESULTS:We showed that genotype 3 HEV could enhance the production of IFN-α/β and induce elevation of ISG15 in C3A cells. HEV ORF3 protein could enhance the production of IFN-α/β and the expression of ISG15. Additionally, ISG15 silencing enhanced the production of IFN-α/β. Overexpression of ISG15 resulted in the reduction of IFN-α/β.CONCLUSION:HEV may promote production of IFN-α/β and expression of ISG15 via ORF3 in the early stages, and increased ISG15 subsequently inhibited the production of IFN-α/β.

Objective:To study the effect of genotype 3 hepatitis E virus ORF3 protein onthe production of type Ⅰ interferon and ISG15 protein in Human hepatocellular carcinoma cells.Methods:Hepatocellular carcinoma cell line PLC-PRF-5 was respectively transfected with the genotype Ⅲ hepatitis E virus ORF3 plasmid and the empty plasmid.At different time points after transfection(0h,8h,12h,24h,48h,72h,120h),the production of IFN Ⅰ in supernatants was measured by ELISA and the expression of ISG15 protein was assayed by Western blot.Results:The levels of IFN α and β3 in the ORF3 plasmid groupsupernatant were obviously higher than those in the empty plasmid group and blank group,but there was no significant change in the empty plasmid group and blank group.And the expression of ISG15 protein was increased in ORF3 plasmid group,but there was no significant change in the empty plasmid group and blank group.Conclusion:Genotype Ⅲ HEV ORF3 protein promotes the expression of type Ⅰ interferon (IFN α and IFN β) and ISG15 protein.

BACKGROUND:Several studies have reported a renoprotective effect of telbivudine during the treatment of patients for chronic hepatitis B (CHB).OBJECTIVES:This longitudinal retrospective study aimed to examine the effects of telbivudine monotherapy and combination therapy (adefovir plus telbivudine) on renal function.PATIENTS AND METHODS:This study included 336 Chinese CHB patients, who were selected from outpatients in Tongji Hospital. 44, 122, 66, 58, and 46 of these patients had been orally taking adefovir, telbivudine, entecavir, adefovir plus telbivudine, and adefovir plus lamivudine, respectively, for at least 24 months.RESULTS:The estimated glomerular filtration rate (eGFR) in the telbivudine and adefovir plus telbivudine groups increased by 5.14 mL/min (P < 0.001) and 6.19 mL/min (P = 0.005), respectively. The patients taking the five drug regimens were further grouped into the following three subpopulations: those with compensated hepatic cirrhosis, those aged 50 or more years, and those with baseline eGFR values of 50 - 90 mL/min. The three subgroups that received telbivudine monotherapy exhibited eGFR increases of 6.38, 6.74, and 10.82 mL/min, respectively. The three subgroups that received combination therapy of adefovir plus telbivudine exhibited eGFR increases of 18.31, 14.73, and 16.59 mL/min, respectively (P < 0.05). The predictive factors for the change in eGFR levels over time were analyzed by means of two linear mixed effects models for the three monotherapy regimens and two combination regimens. Age, gender, and medication are predictive factors of eGFR changes. In addition, abnormal creatinine kinase (CK) levels in the telbivudine group were not correlated with eGFR changes (P = 0.992).CONCLUSIONS:These findings indicate that telbivudine, used in both monotherapy and combination therapy, improves the renal function of patients with CHB. The improvements are particularly significant in patients at high renal risk.

Although rare, acute liver failure (ALF) is associated with high levels of mortality, warranting the development of novel therapies. Nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) play roles in ALF. Lipoxin A4 (LXA4) has been shown to alleviate inflammation in non-hepatic tissues. In the present study, we explored whether LXA4 exerted hepatoprotective effects in a rat model of ALF. A rat model of ALF was generated by intraperitoneal injections of D-galactosamine (300 mg/kg) and lipopolysaccharide (50 µg/kg). Animals were randomly assigned to: control group (no ALF); model group (ALF); and the groups treated with a low dose (0.5 µg/kg), medium dose (1 µg/kg), and high dose (2 µg/kg) of LXA4 (all with ALF); and pyrrolidine dithiocarbamate (PDTC)-treated group (ALF and 100 mg/kg PDTC, an inhibitor of NF-κB). Liver histology was measured using H&E staining, serum levels by ELISA, and liver mRNA expression was measured by RT-PCR for the detection of the pro‑inflammatory cytokines TNF-α and IL-6. Liver cell apoptosis (as measured using the TUNEL method and examining caspase-3 activity), and Kupffer cell NF-κB activity [using an electrophoretic mobility shift assay (EMSA)] were examined. Serum levels of transaminases, TNF-α and interleukin-6 (IL-6) were substantially higher in the model group compared to controls. In the model group, significant increases in TNF-α and IL-6 mRNA expression, TUNEL‑positive cells, and caspase-3 activity in the liver tissue were noted. LXA4 improved liver pathology and significantly decreased the indicators of inflammatory response and apoptosis in a dose-dependent manner. High-dose LXA4 provided better protection than PDTC. LXA4 administration significantly decreased NF-κB expression in hepatocytes and Kupffer cells. These results indicated that LXA4 inhibited NF-κB activation, reduced the secretion of pro-inflammatory cytokines, and inhibited apoptosis of liver cells, thereby exerting protective effects against ALF.

Objective To investigate the role of interleukin-25 (IL-25) in acute liver failure in vivo. Methods An D-galactosamine and lipopolysaccharide-induced acute liver failure in mice was established. The relative levels of IL-25 and interleukin-17 receptor B (IL-17RB) messenger RNA in livertissues of mice were detected by real-time PCR and the IL-25 levels in homogenates of mice liver tissues was detected by enzyme-linked immunosorbent assay. Results The relative levels of IL-25 and IL-17RB mRNA in mice with acute liver failure [(18.05±2.46) and(1.89±0.4)] were significantly higher than in the controls (P<0.05);the levels of IL-25 in liver tissue supernatants of mice with acute liver failure were (26.17 ±14.00) pg/ml,significantly higher than that in the controls [(12.50 ±4.68) pg/ml,P<0.05]. Conclusion IL-25 may play an important role in the pathogenesis of acute liver failure.

AIM:To assess the effects of hepatitis B virus (HBV) on the expression of host α-1,2-mannosidases and determine the underlying mechanisms.METHODS:We measured the expression levels of MAN1A1, MAN1A2, MAN1B1, and MAN1C1 in cell lines HepG2.2.15, HepN10, HepAD38 and HepG2 by Western blot. Viral antigens (HBsAg and HBeAg) in the culture medium were measured using the chemiluminescence method. HBV DNA quantification assays were performed using a commercial real-time PCR kit. Protein levels of human liver tissue α-1,2-mannosidases were also evaluated by Western blot. Plasmids containing seven individual viral genes of HBV (PTT22-HBx, PTT22-HBs, PTT22-preS2, PTT22-preS1, PTT22-HBc, PTT22-HBe, and PTT22-HBp) or control plasmids (PTT22-vector) were transfected into HepG2 cells. MK886 (PPARα) and GW9662 (PPARγ) inhibitors were used to explore the effects of HBV on α-1,2-mannosidase expression after the PPARα and PPARγ pathways were blocked.RESULTS:We showed that the expression of α-1,2-mannosidases was higher in stably transfected HBV cells than in controls. The expression levels of α-1,2-mannosidase were higher in AD38 cells than those in ND10 cells, which were in turn greater than those in G2.2.15 cells, and positively correlated with the expression of HBsAg in all the cell lines. Levels of α-1,2-mannosidase in non-tumorous liver tissues of HBV-related HCC patients were also higher than in the tissues from non-HBV-related HCC patients. Moreover, transfecting HepG2 cells with a component of the HBV viral envelope also increased the expression of α-1,2-mannosidases. However, this envelope protein component could not induce MAN1C1 expression in the presence of a PPARα inhibitor, MK886. We also found that MK886 did not affect the expression of MAN1C1 in AD38 cells without tetracycline in the culture medium. This phenomenon was not observed in the case of GW9662.CONCLUSION:Our results indicate that HBV increases the expression of α-mannosidases both in vitro and in vivo via activation of the PPARα pathway by its envelope protein.

Bacterial resistance to antibiotics is currently a serious health concern.According to the data from the surveil-lance of bacterial resistance in China ( CHINET) ,the isolation rates of gram-negative bacteria have been rising annually. Among the gram-negative organisms, the isolation rate of Carbapenem-resistant enterobacteriaceae, especially extensive drug-resistant strains,has been increasing rapidly.The isolation rate of extensive drug-resistant or pandrug-resistant non-fermenting bacteria,es-pecially Acinetobacter baumanii,is still relatively high.These extensive drug-resistant gram-negative bacteria cause high mortality, which has drawn great attention in clinical settings.On the part of multidrug-assistant gram-positive bacteria,the isolation rate of vancomycin-resistant enterococci remains stable but rates of methicillin-resistant Staphylococcus aureus and coagulase-negative staphylococci are still high.Staphylococcal strains have not yet been found resistant to vancomycin in China.Understanding the epi-demiology of local drug-resistant bacteria facilitates the development of appropriate antibiotic strategies. The mortality of patients with severe infection may be improved by early use of antibiotics and appropriate de-escalation therapy.Rational use of antibiotics and recognition of the influence factors,such as antibiotic-induced endotoxin release,may maximize the efficacy of antibiotics and minimize the adverse reactions.

Hepatitis E virus (HEV) genotype 1 infection is common and can emerge as outbreaks in developing areas, thus posing a threat to public health. However, due to the absence of feasible animal models, the mechanism of HE pathogenesis remains obscure. The HEV pathogenic mechanism has been suggested to be mediated by the immune system and not by direct viral duplication. We firstly discovered that the open reading frame 3 (ORF3) protein of genotype 1 HEV downregulates TLR3-mediated NF-κB signaling in Human A549 Lung Epithelial Cells (A549 cells) which were exposed to different TLR agonists associated with viral nucleic acids. Additionally, we identified the P2 domain of ORF3 as being responsible for this inhibition. Intriguingly, tumor necrosis factor receptor 1-associated death domain protein (TRADD) expression and receptor-interacting protein kinase 1 (RIP1) K63-ubiquitination were reduced in the presence of both ORF3 and Poly(I:C). Furthermore, we found that Lys377 of RIP1 acts as the functional ubiquitination site for ORF3-associated inhibition. Overall, we found that ORF3 protein downregulates TLR3-mediated NF-κB signaling via TRADD and RIP1. Our findings provide a new perspective on the cellular response in HEV infection and expand our understanding of the molecular mechanisms of HEV pathogenesis in innate immunity.

重型肝炎是肝细胞短期内大片坏死或严重变性导致肝功能衰竭的一类危重综合征,包括黄疸进行性加深、凝血功能障碍、肝性脑病和腹水等,其特点是进展迅速、病情凶险、并发症多、预后差,常可导致多器官功能衰竭而死亡,病死率高达50％～80％[1].为和国际接轨,我国已将重型肝炎更名为肝衰竭,包括急性肝衰竭、亚急性肝衰竭、慢加急性肝衰竭和慢性肝衰竭四种类型.

Dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) is an essential process for virus infection, such as HIV and hepatitis C, and plays a role in immune escape. However, the role of DC-SIGN in hepatitis B virus (HBV) infection is still unknown. The aim of this study was to investigate the role of DC-SIGN in mediating the maturation and activation of dendritic cells (DCs) when infected by HBV. Highly mannosylated HBV particles were obtained by treating HBV-producing HepG2.2.15 cells with the a-mannosidase I-inhibitor kifunensine. Highly mannosylated HBV or wild type HBV was added to infect the DCs of the DC-SIGN gene-silencing group and normal group, respectively. Then, the expression of CDla, CD80, CD83, CD86 and HLA-DR on DCs was detected by flow cytometry, the capacity of stimulating lymphocyte proliferation was tested by MTT assay, the level of IL-12p70 that was released by DCs was measured by enzyme-linked immunosorbent assay, and the expression of the proteins NF-κBp65 and p38 was detected by western blot. Both wild type and highly mannosylated HBV could promote DCs maturation and activation. However, the highly mannosylated HBV could promote DCs immune activation more strongly. The difference in the effect on DCs between the two types of HBV could be eliminated by DC-SIGN gene silencing. DC-SIGN can promote the maturation and activation of DCs when recognized HBV, but wild type HBV can escape recognition by DC-SIGN to a certain extent with the help of demannosylated modification, leading to defective DCs function and chronic HBV infection.

Objective To investigate non-bioartificial liver’s influence on clinical efficacy and prognosis of patients with chronic hepatitis B related liver failure.Methods 308 cases of patients who hospitalized in Tongji Hospital(Wuhan)were analyzed in perspective clinical study.Patients who accepted both non-bioartificial liver and standard medical treatment were defined as ALSS group.The ones who accepted standard medical therapy only were defined as SMT group.Taking 8-week as an observation point,we recorded patients’symptoms and biochemical parameters,such as liver function and clotting function.According to them,we could determine the clinical efficacy of patients.Taking the time when patients admitted to hospital and accepted treatment as a starting point,and we took 48 weeks as ending point and recorded the survival time of cases.We took advantage of SPSS 17.0 statistical software to make survival curve and by which to determine the prognosis of our patients with liver failure.The difference of survival rate between two groups was compared by Log Rank test.Results Non-bioartificial liver could improve clinical symptoms and signs,liver function and coagulation function of patients with liver failure (comparing with pre-artificial liver,the level of ALT、TBil were reduced by 63.6 U /L and 34.17 μmol/L respectively,PTA was increased by 7.71% average,P <0.01 ).At 8-week,the difference of clinical efficiency between ALSS group and SMT group was of statistical significance(52.07% vs 34.07%,P <0.01).12-week cumulative survival rate of ALSS group and SMT group were 50.4% and 42.1% respec-tively,the difference between them was not statistical significant(P >0.05).After following up one year, the average survival time of patients in ALSS group was(186.2 ±11.5)days while it was(160.3 ±19.0) days in SMT group patients.The difference of one year cumulative survival rate between two groups was not statistical significant (44.3% vs 40.7%,P >0.05 ).Conclusion Non-bioartificial liver could improve clinical efficiency,while it could not improve prognosis.

Objective:To investigate non-bioartificial liver's influence on clinical efficacy and prognosis of patients with chronic hepatitis B related liver failure,and explore its intervention time for liver failure.Methods:Three hundred and eight cases of patients who hospitalized in Tongji Hospital ( Wuhan) were analyzed in perspective clinical study.Patients who accepted non-bioartificial liver and standard medical treatment were defined as ALSS group.The ones who only accepted standard medical therapy were defined as SMT group.Both of the two groups were divided into three groups of early,medium and advanced stage respectively.Results:At 8-week,the difference of clinical efficien-cy of ALSS group was better than SMT group (52.07%vs 34.07%, P=0.004).The difference of 12-week cumulative survival rate of ALSS group and SMT group was not statistical significant (50.4%vs42.1 %,P>0.05).The result was similar to 48-week cumulative survival rate (44.3%vs 40.7%, P>0.05) .12-week cumulative survival rate of early,medium and advanced stage patients in ALSS group was 81.8%, 62.3%and 14.9%respectively,while 48-week cumulative survival rate of them was 72.7%,56.7%and 9.6%respectively.12-week cumu-lative survival rate of early,medium and advanced stage patients in SMT group was 79.4%,42.9%and 15.3% respectively,while 48-week cumulative survival rate of them was 73.3%,42.9%and 12.3%respectively.Comparing ALSS with SMT group,12-week cumulative survival rate of early stage patients was no statistical significant difference (P>0.05), while the difference of 48-week cumulative survival rate was&nbsp;no statistical significant (P>0.05).The results were the same to advanced stage patients.However,both 12-week cumulative survival rate and 48-week cumulative survival rate of medium-term patients in ALSS group were higher than that of SMT group ( P<0.05) .Conclusion:Non-bioartificial liver could improve clinical efficiency and increase survival rate of patients with liver failure in medium term.But to patients in early stage or advanced liver failure,the value of non-bioartificial liver was little.

Hepatitis B virus (HBV) has been reported to be recognized by dendritic cell-specific ICAM-3-grabbing nonintegrin in the presence of the α-mannosidase I inhibitor kifunensine, whereas native HBV is not. The aim of our study was to determine whether changes in α-mannosidase I expression in peripheral blood mononuclear cells (PBMCs) occur in patients with HBV infection. Peripheral blood was collected from 90 HBV-infected patients (grouped into immune tolerance, chronic hepatitis B, or inactive carrier group based on their clinical states) and 30 healthy donors. Expression of the three α-mannosidase I subtypes, MAN1A1, MAN1A2, and MAN1C1, was measured using western blot analyses. Compared with the healthy controls, significant increases in the MAN1A1, MAN1A2, and MAN1C1 expression levels were observed in the three HBV-infected groups, among whom the immune tolerance group showed the largest increase. For the patients in the immune tolerance phase, the expression levels of both MAN1A1 and MAN1A2 were linearly and positively correlated with the hepatitis B e antigen (HBeAg) titer and HBV DNA level, although a positive correlation was only found between MAN1C1 expression and the HBeAg titer. These results indicate that increased α-mannosidase I expression in PBMCs may play an important role in HBV immune escape and that its expression level is closely related to viral replication activity.

Objective:To investigate whether HBV infection would increase the activity of Golgi MⅠin Hep G2 cell line. Methods:Hep G2 cells and Hep G2.2.15 cells were cultured,and Golgi complexes of these cells were purified by sucrose density gradient centrifugation.The activity of Golgi MⅠin Golgi complexes was detected by colorimetric method. The m RNA expression of MAN1A1、MAN1A2 and MAN1C1 was performed by RT-PCR method. The protein expression of MAN1A1、MAN1A2 and MAN1C1 was performed by Western blot method. Results:It was found that the activity of Golgi MⅠincreased,the m RNA and protein expression of MAN1A1 and MAN1A2 increased too in Hep G2.2.15 cells compared with Hep G2 cells,but there was no difference in the m RNA and protein expression of MAN1C1 between two groups. Conclusion:HBV infection could increase the activity of Golgi MⅠ by up-regulating the m RNA and protein expression of MAN1A1 and MAN1A2.