• Asian Pacific Journal of Cancer Prevention
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• v.16 no.8
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• pp.3479-3483
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• 2015

Objective: Patients with hepatocellular carcinoma (HCC) in stage Barcelona Clinic Liver Cancer (BCLC)-A were grouped based on whether they were accompanied with hepatitis B virus (HBV) infection or not so as to explore the clinical characteristics and prognostic conditions of HCC patients with non-HBV/hepatitis C virus (HCV). Materials and Methods: Clinical data of 64 stage BCLC-A HCC patients with non-HBV/HCV infection (observation group) who received radical hepatectomy in the Affiliated Cancer Hospital of Guangxi Medical University from January, 2006 to November, 2014 were retrospectively analyzed and compared with those of 409 stage BCLC-A HCC patients with HBV infection (control group) in corresponding period. Results: The postoperative 1-, 3- and 5-year recurrent rates of the observation group were 25%, 38.6% and 48.8%, with postoperative mean and median disease-free survival time being 49.1 months and 62.0 months, respectively. Additionally, the postoperative 1-, 3- and 5-year survival rates of observation group were 90.1%, 72.7% and 62.0%, with the mean and median survival times being 54.4 months and 70.0 months, respectively. Conclusions: The 1-year recurrent rate is the highest in HCC patients with non-HBV/HCV, and almost half of the patients have recurrence within 1 year, after which the recurrent rate decreases along with the time.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4199-4202
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• 2015

Background: Hepatitis B virus infection is one of the major world health problems. Epigallocatechin-3 gallate is the major component of the polyphenolic fraction of green tea and it has an anti-viral, anti-mutagenic, anti-tumorigenic, anti-angiogenic, anti-proliferative, and/or pro-apoptotic effects on mammalian cells. In this study, our aim was to investigate the inhibition of HBV replication by epigallocatechin-3 gallate in the Hep3B2.1-7 hepatocellular carcinoma cell line. Materials and Methods: HBV-replicating Hep3B2.1-7 cells were used to investigate the preventive effects of epigallocatechin-3 gallate on HBV DNA replication. The expression levels of HBsAg and HBeAg were determined using ELISA. Quantitative real-time-PCR was applied for the determination of the expression level of HBV DNA. Results: Cytotoxicity of epigallocathechin-3-gallate was not observed in the hepatic carcinoma cell line when the dose was lower than $100{\mu}M$. The ELISA method demonstrated that epigallocatechin-3 gallate have strong effects on HBsAg and HBeAg levels. Also it was detected by real-time PCR that epigallocatechin-3 gallate could prevent HBV DNA replication. Conclusions: The obtained data pointed out that although the exact mechanism of HBV DNA replication and related diseases remains unclear, epigallocatechin-3 gallate has a potential as an effective anti-HBV agent with low toxicity.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3381-3384
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• 2016

Background: Hepatitis B virus (HBV) is a key factor for hepatocellular carcinoma (HCC). About 350 million people are affected by chronic infection which is related to the rapid development of liver diseases as well as hepatitis, cirrhosis and hepatocellular carcinoma. Expression of tumor necrosis factor alpha (TNF-${\alpha}$) in the liver demonstrates a major genetic polymorphism which is involved in resistance or susceptibility to chronic HBV infection. Materials and Methods: In this study, two populations were studied by the sequence specific primer-polymerase chain reaction (SSP-PCR) method: HBV cases (n=409), who were HBS-Ag+, and healthy controls (n=483). Results: The results shown that the frequency of TNF-${\alpha}$ -308 G/G genotype in healthy controls (47.2%) was significantly higher than in HBV infected patients (28%) (CI = 1.29-2.61, OR = 1.83, P = 0.0004). Also TNF-${\alpha}$ -308 A/A and A/G genotype frequencies in the healthy controls were 4.6% and 48.2% and in patient group were 19.5% and 52.5% (CI = 2.23-7.12, p: 0.0001, OR: 3.94) respectively. Conclusions: We found that among Iranian people TNF-${\alpha}$ -308A allele not only has the highest genotype frequency but also it has the highest frequency in the world population. In addition, TNF-${\alpha}$-308 G/G polymorphism was associated with HBV resistance, whereas TNF-${\alpha}$-308A (A/A or A/G) polymorphism appeared to associated with chronic HBV infection. These data suggested that among the Iranian population, the -308 G/G polymorphism of TNF-${\alpha}$ gene promoter region has the potential to influence the susceptibility to HBV infection and it may be responsible for viral antigen clearance.

• Parasites, Hosts and Diseases
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• v.52 no.1
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• pp.47-49
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• 2014

Turkey remains an intermediate area for prevalence of hepatitis B virus (HBV) surface antigenemia. The sheep-raising areas of Turkey also pose a high risk for cystic hydatid disease (CHD). Both HBV infection and CHD are major public health issues particularly in eastern parts of Turkey; however, there is no data regarding HBV infection in patients who have had CHD. The aims of this study were to evaluate the association between HBV infection and CHD and suggest ways to reduce HBV infection which is still widespread in Turkey. A retrospective study was conducted with 94 adult patients with active CHD referred to the hepatology department, Yuzuncuyil University School of Medicine from December 2010 to December 2012. All subjects came from rural areas of the region and underwent ultrasonography of abdomen which detected CHD of the liver. All the patients were serologically positive for Echinococcus granulosus. The control group consisted of 500 patients (300 men and 200 women) referred to the internal medicine clinics for other reasons. The patients with CHD and in the control group were tested for the existence of HBs antigen according to the standard procedures. The seroprevalence of HBs antigen was significantly higher in patients with active CHD than those in the control group (12.7% vs 5.2%; P=0.0017). Our data indicate that there is significant association between HBV infection and CHD. All patients with CHD should be screened for HBV infection.

• Archives of Pharmacal Research
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• v.29 no.11
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• pp.1042-1048
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• 2006

Plasmid DNA vaccines encoding the hepatitis B virus (HBV) surface and hepatitis C virus (HCV) envelope antigens, respectively, were constructed, and attempt were made to find the possibility of a divalent vaccine against HBV and HCV. The expression of each plasmid in Cos-1 cells was confirmed using immunocytochemistry. To measure the induced immune response by these plasmids in vivo, female BALB/c mice were immunized intramuscularly with $100\;{\mu}g$ of either both or just one of the plasmids. Anti-HBV and HCV-specific antibodies and related cytokines were evaluated to investigate the generation of both humoral and cellular immune responses. As a result, specific anti-HBV and anti-HCV serum antibodies from mice immunized with these plasmids were observed using immunoblot. The levels of IL-2 and RANTES showing a $Th_{1}$ immune response were significantly increased, but there was no change in the level of IL-4 ($Th_{1}$ immune response) in any of the immunized groups. Compared with each plasmid DNA vaccine, the combined vaccine elicited similar immune responses in both humoral and cell-mediated immunities. These results suggest that the combined DNA vaccine can induce not only comparable immunity experimentally without antigenic interference, but also humoral and $Th_{1}$ dominant cellular immune responses. Therefore, they could serve as candidates for a simultaneous bivalent vaccine against HBV and HCV infections.

• Journal of Life Science
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• v.17 no.6 s.86
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• pp.766-771
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• 2007

The co-infection with hepatitis B virus (HBV) and hepatitis C Virus (HCV) is associated with a more severe liver disease and increased frequency in the development of hepatocellular carcinoma com-pared to those with single infection. Here, we demonstrated that HBV X protein (HBx) and HCV Core cooperatively up-regulated the level of p53 in human hepatoma HepG2 cells. The elevated p53 subsequently stimulated the expression of proapoptotic Bax whereas it repressed the expression of antiapoptotic Bcl2. These effects, however, were not observed in p53-negative Hep3B cells. Consistently to their cooperative regulation of apoptotic effectors, HBx and HCV Core additively stimulated cisplatin-mediated apoptotic cell death of HepG2 but not of Hep3B cells. These results may help to explain the development of a more severe liver disease in patients co-infection with HBV and HCV as well as some contradictory results on the roles of HBx and Core in apoptosis.

• Childhood Kidney Diseases
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• v.2 no.1
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• pp.50-59
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• 1998

Purpose : Hepatitis B virus (HBV) infection has been involved in several forms of immune-related glomerulopathy but the pathogenic role of HBV infection is not clear. To evaluate the clinicopathological features of HBV-associated glomerulopathy, a clinicopathological analysis and immunohistochemical stain for HBs Ag and HBe Ag were done. Methods : Clinicopathological features of HBV-associated glomerulopathy were analyzed with renal biopsies in 28 HBsAg seropositive patients from April 1990 to February 1997 at Pusan Paik Hospital, and immunohistochemical evaluation for HBsAg and HBeAg was done in renal tissues. Light microscopic, immunofluorescent and electron microscopic examination and immunohistochemical staining for HBsAg (DAKO) and HBeAg (BIONIKE) of renal tissue were performed. Result ; 1. The age distribution was 6 to 73 years old, and eight were children and 20 were adults. Male : female ratio was 3:1. Nineteen (67.9%) and 21 (75.0%) of 28 cases showed hematuria and proteinuria, respectively at the time of biopsy. Sixteen (57.2%) of them had nephrotic syndrome. 2. Liver function test was performed in 11 patients and seven (63.6%) of them showed increased AST and ALT levels. Liver biopsy was done in three patients and revealed findings of chronic active hepatitis. 3. HBV-associated glomerulopathy was membranous glomerulonephritis (MGN) in 10 (35.7%), mesangiopathy in 8 (28.6%), membranoproliferative glomerulonephritis (MPGN) in 7 (25.0%) and minimal change disease in 3 (10.7%) out of 28 cases. 4. Ultrastructurally HBV-associated MGN showed conspicuous subepithelial deposits with intramembranous, mesangial and subendothelial deposits and proliferation of mesangial cells and matrix, which were suggestive of MPGN. In HBV-associated MPGN, intramembranous and subepithelial deposits were scattered. 5. Immunohistochemical staining revealed no expression for HBsAg, but positive reaction for HBeAg along capillary wall in 8 cases (28.6%), of which 3 cases were checked for serum HBeAg, all showed positivity. Conclusion : HBV-associated glomerulopathy showed a wide morphologic spectrum and overlapping ultrastructural features in MGN and MPGN, and the activity of hepatitis B virus may be related to the development of HBV-associated glomerulopathy but further studies are recommended to confirm this relationship.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.12 no.1
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• pp.23-29
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• 2009

Purpose: To provide the primary data for reaching a consensus on the adequate duration of treatment of lamivudine in children with HBeAg negative chronic hepatitis B. Methods: Seven of 83 children/adolescents with chronic hepatitis B were diagnosed with HBeAg-negative and HBV DNA-positive chronic hepatitis B and treated with lamivudine. Six children/adolescents were enrolled among 7 patients, who had been treated with lamivudine over 2 years. The primary goal of treatment was HBV DNA clearance and normalization of the serum ALT level; the final goal of treatment was the durability of the complete response after discontinuation of lamivudine. It was planned to continue lamivudine for more than two additional years after HBV DNA negativity and normalization of ALT. Results: The mean duration of lamivudine treatment was 32.2 months (range, 26~40 months) and the mean duration of follow-up was 59.5 months (range, 26~110 months). HBV DNA levels became undetectable (<0.5 pg/mL) in 6 patients within 3 months of treatment. ALT levels were normalized in 3.5 months (range, 2~7 months) in all 6 patients. Biochemical breakthrough developed in 1 patient 18 months after the initiation of lamivudine treatment. No evidence of relapse could be found in 4 patients with a mean follow-up of 23.8 months (range, 4~75 months) after cessation of lamivudine treatment. Conclusion: Suppression of HBV replication and normalization of serum ALT levels were effectively achieved with long-term lamivudine treatment in children/adolescents with HBeAg-negative chronic hepatitis B. Two additional years of lamivudine may be needed after HBV DNA clearance and ALT normalization in HBeAg-negative chronic hepatitis B in order to decrease the relapse rate.

• Journal of Microbiology and Biotechnology
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• v.18 no.10
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• pp.1722-1728
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• 2008

The natural course of chronic hepatitis B (CH-B) virus infection is reportedly variable, and the long-term outcomes in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B infection are distinct from HBeAg-positive chronic hepatitis. However, the molecular virological factors that contribute to the progression of liver disease in the south Indian setting remain largely unclear. We prospectively studied 679 consecutive patients for HBsAg, HBeAg, anti-HBe, and HBV DNA by qualitative PCR. Randomly selected samples were subjected to bidirectional sequencing to reveal core/precore variants. Of the total 679 chronic HBV cases investigated, 23% (154/679) were replicative HBV carriers. Furthermore, amongst the 560 HBV DNA samples analyzed, 26% (146/560) were viremic. Among the 154 HBeAg positive cases, HBV DNA was positive in 118 cases (77%), significantly (p<0.001) higher than the anti-HBe positive (7%) (28/406) cases. Significant increase in liver disease (p<0.01) with ALT enzyme elevation (p<0.001) was observed in both HBe and anti-HBe viremic cases. Interestingly, low frequencies of mutations were seen in the precore region of the HBV strains studied. HBV precore and core promoter variants were less often detected in subjects with "e" negative chronic HBV infection and, therefore, may not have a prognostic role in determining liver disease sequelae in this part of tropical India.

• Journal of Preventive Medicine and Public Health
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• v.33 no.3
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• pp.323-333
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• 2000

Objectives : Chronic HBsAg carriers are the principal source of infection for other susceptible people, and are themselves at high risk of developing serious liver diseases. In Korea, it has been estimated that 65-75% of the HBsAg positives remained as persistent carriers. Additionally, familial clustering of MBV infection has frequently been observed among carriers. Some would become progressive, chronic hepatitis patients, and others would not. The aim of this study was to evaluate the association between various factors, such as the duration of infection, type of virus, mutation of precore/core region in HBV, major histocompatibility class-I, and developing chronic liver diseases among familial HBV carriers. Methods : Chronic carrier status was identified by repeated serological tests for HBsAg at intervals of six months or more. A familial chronic carrier was defined when the disease was observed in a family member over two generations. Two families were recruited, among which a total of 20 chronic HBsAg carriers(11 carriers in No.1, and 9 in No.2 family) were identified. Data on the general characteristics and liver disease status were collected. Identification of the HBV-DNA was successful only for 13 subjects among the 20 carriers. Analysis of viral DNA in terms of subtype, pre-core and core region mutations was carried out. The type of major histocompatibility class-1 for the 13 subjects was also analysed. Results & Conclusions : Seven of 10 chronic HBV carriers of the 1st generation and one of 10 of the 2nd generation were clinical patients with chronic hepatitis, the others, three of the 1 st and nine of the 2nd generation, were asymptomatic carriers. This data indicates that the duration of HBV carriage is one of the major factors for disease severity. The subtype of HBsAg analysed using MBV-DNA identified in 13 carriers were adr, and the pattern of precore nonsense mutation in HBV-DNA was identical among family members, which meads that the same virus strains were transmitted between the family members. The association between the precore or core mutations in HBV-DNA and the disease severity was not observed. While it was suggested that a specific type of MHC class-I may be related to disease progression.