• 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.

• Journal of Applied Biological Chemistry
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• v.59 no.1
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• pp.25-29
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• 2016

Hepatitis B virus infection can cause hepatic fibrosis leading to cirrhosis and hepatocellular carcinoma. However the mechanism remains poorly understood. In this study, we found that Hepatitis B virus X-protein (HBx) increases vimentin, fibronectin, slug, snail and NOX4 expression. Because NOX4-mediated reactive oxygen species can increase slug and snail, which can induce fibrosis, HBx may be a key regulator of hepatic fibrosis development via NOX4 induction.

• Korean System Dynamics Review
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• v.7 no.2
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• pp.215-226
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• 2006

A conceptual system dynamics model is developed to represent the dynamic mechanism between the number of hepatitis B virus and the defense system of the body. The simulation results shows that the model behaves within the reasonable ranges. The developed conceptual model is a first attempt to quantify the dynamic mechanisms of the hepatitis B virus, where only feedback structures are considered without bio-organism data. The next step would be to incorporate the model with bio-organism theory and to carry out case studies to identify personal characteristics. Since the current model is a conceptual model where quantitative results are not based on the sound background, the usage is limited only within the qualitative basis. It could be a effective educational tool for the patients. It also shows what-to-do lists in order to be used for forecast purposes.

• Korean Journal of Microbiology
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• v.49 no.3
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• pp.221-227
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• 2013

Human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV) cause viral infections that lead to chronic diseases. When they invade human body, virus specific T cells play an important role in antiviral effector functions including killing virus-infected cells and helping B cells to produce specific antibodies against viral proteins. The antiviral activity of T cells is usually affected by immune-regulatory factors that express on surface of T cells. Recently, many researchers have investigated the relationship between effector functions of virus specific T cells and characteristics of immune regulatory factors (e.g., CD28, CD25, CD45RO, FoxP3, PD-1, CTLA-4). In particular, Immune inhibitory molecules such as forkhead box P3 (FoxP3), programmed death-1 (PD-1), and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) are associated with T-cell dysfunction. They are shown to be up-regulated in chronic viral diseases such as hepatitis B, hepatitis C or human immunodeficiency virus infection. Therefore, the positive correlation between viral persistence and expression of immune regulatory factors (FoxP3, PD-1, and CTLA-4) has been suggested. In this review, the roles of immune regulatory factors FoxP3, PD-1, and CTLA-4 were discussed in chronic viral diseases such as HIV, HBV, or HCV.

• IMMUNE NETWORK
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• v.15 no.4
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• pp.191-198
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• 2015

Hepatitis B virus (HBV) is responsible for approximately 350 million chronic infections worldwide and is a leading cause of broad-spectrum liver diseases such as hepatitis, cirrhosis and liver cancer. Although it has been well established that adaptive immunity plays a critical role in viral clearance, the pathogenetic mechanisms that cause liver damage during acute and chronic HBV infection remain largely known. This review describes our current knowledge of the immune-mediated pathogenesis of HBV infection and the role of immune cells in the liver injury during hepatitis B.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.82-82
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• 1997

The hepatitis B virus(HBV) is a small, enveloped virus with a circular, double-stranded DNA genome. HBV causes active and chronic hepatitis worldwide, including Korea, and is considered to be a major factor for liver cirrhosis and hepatocellular carcinoma. In contrast to the wealth of knowledge on the gene structure and expressional regulation, immunological and pathological mechanisms for HBV-induced hepatocellular injury are not well known. In the present study, vaccinia virus which has been demonstrated to be a useful eukaryotic expression vector was used to clone the gene for HBV surface antigen, L(S+preS2+preS1). The recombinant vaccinia virus vector, pMJ-L, which contains L surface antigen gene of adr-type HBV was constructed, and subseouently used for making recombinant vaccinia virus VV-$\textrm{HBV}_{L}$. Expression of the HBV antigen was examined by immunofluorescent antibody (IFA) test using mouse monoclonal anti-hepatitis B surface antigen. HBsAg was detected in the recombinant virus indicating that the VV-$\textrm{HBV}_{L}$ expressed S antigen successfully. The HBV-Vaccinia Virus recombinant obtained in this study is currently being used for studying the immunological aspects of HBV infection.

• Molecules and Cells
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• v.28 no.1
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• pp.49-55
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• 2009

Hepatitis delta virus (HDV) infection causes fulminant hepatitis and liver cirrhosis. To elucidate the molecular mechanism of HDV pathogenesis, we examined the effects of HDV viral proteins, the small hepatitis delta antigen (SHDAg) and the large hepatitis delta antigen (LHDAg), on $NF-{\kappa}B$ signaling pathway. In this study, we demonstrated that $TNF-{\alpha}-induced$ $NF-{\kappa}B$ transcriptional activation was increased by LHDAg but not by SHDAg in both HEK293 and Huh7 cells. Furthermore, LHDAg promoted TRAF2-induced $NF-{\kappa}B$ activation. Using coimmunoprecipitation assays, we demonstrated that both SHDAg and LHDAg interacted with TRAF2 protein. We showed that isoprenylation of LHDAg was not required for the increase of $NF-{\kappa}B$ activity. We further showed that only LHDAg but not SHDAg increased the $TNF-{\alpha}-mediated$ nuclear translocation of p65. This was accomplished by activation of $I{\kappa}B_{\alpha}$ degradation by LHDAg. Finally, we demonstrated that LHDAg augmented the COX-2 expression level in Huh7 cells. These data suggest that LHDAg modulates $NF-{\kappa}B$ signaling pathway and may contribute to HDV pathogenesis.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.11a
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• pp.39-40
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• 1993

Hepatitis B virus (HBV)is a member of the Hepadna virus family whose members share a characteristic virion structure and genome size, around 3.2kb in a paritially double-stranded form. The genome of HBV contains four overlapping open reading frames designated as P(polymerase). C(core), S(surface antigen)and X. The X gene has potential to encode 154 amino acids protein.

• Korean Journal of Clinical Laboratory Science
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• v.36 no.1
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• pp.33-37
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• 2004

In order to study the effect of temperature of denaturation, annealing and extension and cycles on amplification of DNA by PCR method, We isolated the hepatitis B virus DNA from hepatitis B patient blood and compared the density of DNA amplified by Reference PCR Program (denaturation at $94^{\circ}C$ for 30 sec., annealing at $60^{\circ}C$ for 1 min., extension at $72^{\circ}C$ for 1 min., holding at $72^{\circ}C$ for 5min., 30 cycles) that is usually used in laboratory to the density of DNA amplified by PCR program changed only the denaturation temperature or annealing temperature or extension temperature. We amplified about 341bp of hepatitis B virus DNA by Reference PCR Program from hepatitis patient blood, but the DNAs denatured at $72^{\circ}C$ or $60^{\circ}C$ were not detectable on photoradiography film. The DNA amplified at $37^{\circ}C$ of annealing temperature was not detectable, but the DNA annealed at $72^{\circ}C$ was detectable the lower density of DNA than the DNA amplified by Reference PCR Program. Each DNA amplified by PCR program changed only the extension temperature to $37^{\circ}C$ or $60^{\circ}C$ was almost same density as DNA amplified by Reference PCR Program. We compared the density of hepatitis B virus DNA amplified by Reference PCR Program for 30 cycles, 20 cycles, 10 cycles, and 5 cycles. The DNA cycled for 20 cycles was not amplified well as cycled for 30 cycles, but the DNA was detectable on the photoradiography film. The DNAs amplified for 10 cycles or 5 cycles were not detectable on photoradiorgaphy film. The concentration of hepatitis B virus DNA amplified in Reference PCR condition for 30 cycles, 20 cycles, 10 cycles, and 5 cycles were $72{\mu}g/m{\ell}$, $83{\times}10^{-3}{\mu}g/m{\ell}$, $27{\times}10^{-6}{\mu}g/m{\ell}$, and nondetectable, respectively.

• Korean Journal of Microbiology
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• v.43 no.1
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• pp.1-6
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• 2007

We describe a multiplex PCR method that can detect and differentiate simultaneously four different kinds of DNA viruses, Epstein-Barr virus (EBV), cytomegalovirus (CMV), hepatitis B virus (HBV) and parvovirus B19 (B19). Primers for the multiplex PCR reaction were designed to amplify specific regions of the EBV (pol), CMV (pol), HBV (pol) and B19 (ns) viral genomes and used to simultaneously detect individual viruses. In order to achieve optimal sensitivity and specificity for multiplex PCR, the thermo-cycling parameters, primer sequences, and concentration of each reaction components were optimized systematically. The sensitivity of the detection method ranged between 5 and 10 copies of viral genome with a mixture of multiple primer pairs. Furthermore, this highly sensitive test showed no cross-reactivity among the four viruses. Thus, the results obtained in this study provide evidence that the assay system is a good tool for supporting the diagnosis of viral infection and contamination.