• Perspectives in Nursing Science
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• v.7 no.1
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• pp.50-54
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• 2010

The studies of M. Colombo (1989) and W. Lange (1992) showed that 30~40% of people became chronic after suffering from hepatitis B virus (HBV) and C virus (HCV) infection, and about 50% of the chronic cases transformed into primary liver cancer. There have been few studies done in Mongolia on hepatitis infection among health professionals, particularly in nurses. In a study done by Chimedsuren (8), the study showed that 19.4% of people with identified surface hepatitis B antigen (HBsAg) and antibodies to hepatitis C virus and 8% of people with the identified nucleotide of RNA for the hepatitis C virus (polymerase chain reaction) had an acute form of hepatitis C. Studies on the hepatitis virus genome damaging effect on liver cells showed that genotype 8 (A, B, C, D, E, F, G, TTV) had the most damaging effect on liver cells (Hahn and Faeka, 2007). Several studies have shown a relationship between hepatitis B virus infection and a lack of compliance regarding safety regulations and rules by medical personnel. Results of a study from the Maternal and Child Health Research Center showed that tests done to detect hepatitis B virus antigen and antibodies to C virus did not reveal anything. Both antigen and antibodies in 69% cases did not show, and separately, B virus and antibodies to hepatitis C virus were identified in 13% and 9%, respectively. Results of the tests taken from health personnel in Shastin Central Hospital showed that in 76% of the cases, the B virus antigen with C virus antibodies was not identified. In 8% of the cases, the B virus antigen was present on its own. The combination of B the virus antigen and C virus antibodies were present in 8% of nurses and doctors, respectively. 82% of the cases had negative results for the detection of a combination of B virus antigen and C virus antibodies taken from health personnel from the State Central Clinical Hospital whereas the B virus antigen and C virus antibodies by themselves were present in 7% and 14% of the cases, respectively. Combined cases of the B virus antigen and C virus antibodies were identified in 4% of the personnel. Results of the tests taken from the health personnel in the Hospital of the Ministry of Justice and Internal Affairs showed that in 79% of the cases, the B virus antigen with C virus antibodies were not identified. Separately, the B virus and antibodies to hepatitis C virus were identified in 8% and 13% of the cases, respectively.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.16 no.1
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• pp.61-64
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• 2013

Infection-induced acute hepatitis complicated with acute pancreatitis is associated with hepatitis A virus, hepatitis B virus or hepatitis E virus. Although rare, Epstein-Barr virus (EBV) infection should be considered also in the differential diagnosis if the patient has acute hepatitis combined with pancreatitis. We report a case of EBV infection with cholestatic hepatitis and pancreatitis with review of literature. An 11-year-old female was admitted due to 1-day history of abdominal pain and vomiting without any clinical symptoms of infectious mononucleosis. Diagnosis of reactivated EBV infection was made by the positive result of viral capsid antigen (VCA) IgM, VCA IgG, Epstein-Barr nuclear antigen and heterophile antibody test. We performed serologic tests and magnetic resonance cholangiopancreatography to exclude other viral or bacterial infection, autoimmune disorder, and structural problems. The patient's symptoms recovered rapidly and blood chemistry returned to normal with conservative treatment similar to previously reported cases.

• The Journal of Korean Society of Virology
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• v.27 no.2
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• pp.129-135
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• 1997

Serum samples from 123 males and 123 females collected by age in 1996 were analyzed for antibodies against surface antigen of Hepatitis B virus and C22-3, C200 antigens of Hepatitis C virus. Sera from the children under the age of 10 showed 30% seropositivity to the surface antigen of Hepatitis B virus, 33.3% in $10{\sim}19$ year group, 20% in $20{\sim}29$ year group, 17.6% in $30{\sim}39$ year group, 3.3% in $40{\sim}49$ year group, 5.9% in $50{\sim}59$ year group, 8,3% in $60{\sim}69$ year group, 2.9% in $70{\sim}79$ year group, but antibody could not found in $80{\sim}86$ year group. 12 out of 123 male sera were positive, 19 out of 123 female sera were positive and overall rate of positivity of antibody against surface antigen of Hepatitis B virus was 12.6%. Serum samples from peoples under the age of 30 had not antibody against C22-3, C200 antigens of Hepatitis C virus. The positivity rate was 2.9% in $30{\sim}39$ year group. 5 out of 30 sera from $40{\sim}49$ year age group were positive, and 3 positive sera showed extremely high titer (1:524,288) but the titers of two remaining sera were 1:32, 1:8,192 respectively. 5.9% was positive in $50{\sim}59$ year group, 8.3% in $60{\sim}69$ year group, 11.8% in $70{\sim}79$ year group but all negative in $80{\sim}86$ year group 6 out of 123 male sera were positive (4.9%), 9 out of 123 female sera were positive (7.3%). Overall rate of positivity of antibody against C22-3, C200 antigen of Hepatitis C virus was 6.1 %. None out of 246 sera had both antibodies against Hepatitis B virus and Hepatitis C virus.

• Journal of Yeungnam Medical Science
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• v.3 no.1
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• pp.325-332
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• 1986

Since Combes' first description of hepatitis B virus associated membranous glomerulonephritis, many reports have shown a strong association of hepatitis B virus infection with various types of nephropathies, especially membranous glomerulonephritis and membranoproliferative glomerulonephritis. Recently, the authors experienced a case of membraoproliferative glomerulonephritis, type I in a 16-year-old male patient with persistent HBs and HBe antigenemia. One year prior to admission the patient was told of hepatitis at routine check, but he remained asymptomatic throughout. He was admitted to our hospital with chief complaints of proteinuria and microscopic hematuria found on routine urinalysis. Liver and kidney biopsy revealed chronic persistent hepatitis and membranoproliferative glomerulonephritis type I, respectively. We report a case of hepatitis B virus associated nephropathy with review of the literatures. Considering the endemic nature of hepatitis B virus infection in Korea, the incidence of hepatitis B viurs associated nephropathy would be proportionally high in comparison with those of other countries. So, the importance of this entity merits special consideration in our country. Further study concerning pathogenesis, epidemiology, and treatment may be needed.

• Journal of Integrative Natural Science
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• v.9 no.1
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• pp.23-27
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• 2016

Hepatitis B virus is the leading source of liver disorders and is a global health problem and needs advancements in its treatment against increasing problems. Recently five vanitaracin derivatives were isolated from the fungus Talaromyces species which have anti-Hepatitis B virus activity. Hence, in the present study, molecular docking was carried out with five vanitaracin derivatives isolated from Talaromyces species and three known inhibitors.The objective of this work is to study the interaction of newly isolated compounds and compare its interaction with known inhibitors. The docking results revealed that vanitaracin derivatives have good interactions and has better docking score with the Hepatitis B virus and suggest SER2, SER4 and ASP30 are important residues involved in interaction with the inhibitors. These result authenticates vanitaracin derivatives contributes to inhibitory activity of Hepatitis B virus to treat liver disorders.

• Journal of Microbiology and Biotechnology
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• v.27 no.10
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• pp.1727-1735
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• 2017

Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences, such as chronic hepatitis and liver damage, mortality of the latter of which reaches up to 20-30%. Type I interferon (IFN)-induced antiviral immunity is known to be the first-line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors, leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of IFN-stimulated genes, helping the cells cope with viral infection. Interestingly, some of the HEV-encoded genes seem to be involved in disrupting signaling cascades for antiviral immune responses, and thus crippling cytokine/chemokine production. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge, and in this review, we summarize known HEV evasion strategies and compare them with those of other hepatitis viruses.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.1
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• pp.275-279
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• 2013

Objectives: A number of studies have shown that chronic hepatitis B virus infection is implicated in susceptibility to pancreatic cancer. However, the results are still controversial. This meta-analysis aimed to quantitatively assess the relationship between chronic hepatitis B virus infection and incidence of pancreatic cancer of cohort and case-control studies. Methods: A literature search was performed for entries from 1990 to 2012 using PUBMED and EMBASE. Studies were included if they reported odds ratios (ORs) and corresponding 95% CIs of pancreatic cancer with respect to the infection of hepatitis B virus. Results: Eight studies met the inclusion criteria, which included five case-control studies and three cohort studies. Compared with individuals who have not infection of hepatitis B virus, the pooled OR of pancreatic cancer was 1.403 (95%CI: 1.139-1.729, P=0.001) for patients with hepatitis B virus infection. Sub-group analysis by study design showed that the summary OR was 1.43 (95%CI: 1.06-1.94, P=0.021) when pooling case-control studies and 1.31 (95%CI: 1.00-1.72, P=0.05) when pooling cohort studies. Conclusion: Findings from this meta-analysis suggest that chronic hepatitis B virus infection may increase the risk of pancreatic cancer. This relationship needs to be confirmed by further follow-up studies.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4509-4513
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• 2013

Chronic hepatitis B virus (HBV) infection has long been the most common cause of hepatocellular carcinoma (HCC). However, some aspects of the pathogenesis of HBV infection and genesis of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) are still inconclusive. An increasing number of published studies indicate that hepatitis B virus mutations are associated with risk of HCC. These variations include, in particular, mutations in ORF S,C,X gene regions. This mini-review summarizes results of clinical studies and molecular mechanisms on the possible relations of HBV mutations with the development of hepatocellular carcinoma.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.25 no.2
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• pp.229-235
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• 2015

Objectives: We checked hepatitis A virus antibody(anti-HAV IgG) and hepatitis B virus antibody(HBsAb) in three large companies. The result could be a guideline to establish proper health policy for Hepatitis A and B virus preventive plan in company. Methods: We investigated the seroprevalence of anti-HAV IgG and HBsAb, and demographic characteristics of employee volunteer in three companies in southern area of Korea. Company was divided three according to health policy for hepatitis A and B. Results: The seroprevalence rate of anti-HAV IgG in company A, B, and C was 53.6%, 25.8%, and 17.7%(P<0.001), respectively. The seroprevalence rate of HBsAb in workplace A, B, and C was 79.7%, 82.4%, and 70.9%(P<0.001), respectively. Anti-HAV IgG showed more considerable difference among the companies. Conclusions: The results confirmed that low rate of IgG anti-HAV and HBsAb, particularly in the company that had low level of hepatitis education and vaccination program. This study was important for establishing hepatitis education policies, to prevent and control outbreaks in companies.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.5 no.1
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• pp.39-50
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• 2002

Hepatitis B viral infection which affect about 10% of Korean population manifests asymptomatic carrier, chronic hepatitis and liver cirrhosis and even associates with hepatocellular carcinoma. Clinical manifestations induced by hepatitis B virus vary depending on the degree of immune response by cytotoxic T cells against viral epitope-presenting liver cells. Since hepatitis B virus presents high rate of mutaton that might change the presented epitope and eventually alter immune response, viral mutations, especially in promoters and enhancers, have an important implication in hepatic inflammation and viral replication. To identify mutations related to the hepatic inflammation, we investigated sequence variations of hepatitis B viral promotor regions in the presence or absence of symptoms in hepatitis B carriers. For this, sera from persistently hepatitis B virus-infected mother-child pairs were collected. After PCR amplifiation of all hepatitis B viral promoters (C promoter, S1 promoter, S2/S promoter, X promoter) using serum DNA from each pair, viral promotors were sequenced by automatic sequencer and then sequence data were analyzed by ClustalW. In most cases, the dominant type of maternal virus was transmitted to the child. However, in some children, some new host specific viral variants could be observed in Cp, S1p and S2/Sp. The mutations in C promoter did not seem to be vertically transmitted but arose in new host independently after the wild type had been transmitted. Enhancer I containing X promoter revealed high host specific variations as has been reported before. Two S promoters, S1p and S2/Sp, have shown some point mutations in children, but no deletion mutations were detected as in chronic hepatitis patients in whom deletion mutations are frequently found. In conclusion, the children with the vertically transmitted hepatitis B virus mostly retain the dominant type virus that had been transmitted. However, host specific variants tended to accumulate over time, possibly as clinical symptoms develop.