• Title/Summary/Keyword: Viral hepatitis

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KM-based Treatment of Viral Hepatitis A accompanied with Pancreatitis: A case report

  • Son, Chang-Gue
    • The Journal of Korean Medicine
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    • v.41 no.4
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    • pp.106-111
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    • 2020
  • Objectives: Hepatitis A is a typical acute hepatitis caused by hepatovirus, and then most patients recover easily without progression to chronic condition. However, certain cases have the risk of severe symptoms or even death. This case report presented a hepatitis A accompanied with pancreatitis, which had been completely recovered in a Korean medicine hospital. Case presentation: A 38-year woman had felt the malaise, mild chilling, muscle pain and abdominal discomfort for 10 days, which led her visit doctors and took anti-pyretic analgesics and digestants. The symptoms, especially epigastric pain and fatigue, became worse, and then she hospitalized in a Korean medicine hospital. Based on the drastic elevations of hepatic enzymes (aspartate transaminase 1,604 IU/L and alanine transaminase 2,825IU/L) with an anti-HAV IgM positive, she was diagnosed with hepatitis A. After bed rest and herbal drug treatment (CGX and Innae-Tang) for 5 days, the laboratory abnormalities and subjective symptoms had been improved gradually, except the upper gastric discomfort and pain. Those symptoms had anticipated the comorbidity with HAV-induced pancreatitis, supported by the high level of serum lipase release. Another 5-day hospitalized treatment improved all subjective symptoms and then the laboratory results were completely normalized including detection of anti-HAV IgG within 15 days after discharge. Conclusion: This study presented a typical hepatitis A accompanied with pancreatitis, which should be considered in diagnosis and management of hepatitis A.

Immune-mediated Liver Injury in Hepatitis B Virus Infection

  • Oh, In Soo;Park, Su-Hyung
    • 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.

An Outbreak of Viral Haemorrhagic Pneumonia(Tentative Name) of Rabbits in Korea (토끼의 바이러스성 출혈성 폐렴(잠정명칭) 발생)

  • Park Nam-Yong;Chong Chi-young;Kim Jin-ho;Cho Sung-man;Cha Yeon-ho;Jung Byung-tack;Kim Dong-sung;Yoon Ji-byung;Park Jin-yul;Wee Sung-ha
    • Journal of the korean veterinary medical association
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    • v.23 no.9
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    • pp.603-610
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    • 1987
  • The pathological and microbiological studies were carried out to investigate an acute, febrile, highly fetal, infectious disease of rabbits that had occurred in the Winter and in the Spring and that had begun to be reported in Korea from November, 1985. The clinical signs of this disease were characterized by high fever, lethargy, piercing shriek, convulsion, and sudden death with epistaxis, but often they were not observed. The predominant pathogical findings were severe congestion and hamorrhage in trachea, dark brown discoloration of liver by diffuse necrosis or acute viral hepatitis, and hamorrhagic damages of lung, heart, spleen, kidney, etc. The etiological agent was a small round virus, in 25-35nm in diameter and without envelope, thus looking like a picorna virus. This disease resembled what was called the 'Viral Hamorrhagic Pneumonia in Rabbits'(tentative name) that had been reported for the first time in China in 1984. It will be desirable that the disease should be renamed as the 'Viral Hemorrhagic Fever in Rabbits', the 'Acute Viral Hepatitis in Rabbits', etc. because of its charateristics and the basis of pathological findings. An inactivated vaccine is now in the process of preparation for the prophylaxis of this viral disease.

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Nonstructural NS5A Protein Regulates LIM and SH3 Domain Protein 1 to Promote Hepatitis C Virus Propagation

  • Choi, Jae-Woong;Kim, Jong-Wook;Nguyen, Lap P.;Nguyen, Huu C.;Park, Eun-Mee;Choi, Dong Hwa;Han, Kang Min;Kang, Sang Min;Tark, Dongseob;Lim, Yun-Sook;Hwang, Soon B.
    • Molecules and Cells
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    • v.43 no.5
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    • pp.469-478
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    • 2020
  • Hepatitis C virus (HCV) propagation is highly dependent on cellular proteins. To identify the host factors involved in HCV propagation, we previously performed protein microarray assays and identified the LIM and SH3 domain protein 1 (LASP-1) as an HCV NS5A-interacting partner. LASP-1 plays an important role in the regulation of cell proliferation, migration, and protein-protein interactions. Alteration of LASP-1 expression has been implicated in hepatocellular carcinoma. However, the functional involvement of LASP-1 in HCV propagation and HCV-induced pathogenesis has not been elucidated. Here, we first verified the protein interaction of NS5A and LASP-1 by both in vitro pulldown and coimmunoprecipitation assays. We further showed that NS5A and LASP-1 were colocalized in the cytoplasm of HCV infected cells. NS5A interacted with LASP-1 through the proline motif in domain I of NS5A and the tryptophan residue in the SH3 domain of LASP-1. Knockdown of LASP1 increased HCV replication in both HCV-infected cells and HCV subgenomic replicon cells. LASP-1 negatively regulated viral propagation and thereby overexpression of LASP-1 decreased HCV replication. Moreover, HCV propagation was decreased by wild-type LASP-1 but not by an NS5A binding-defective mutant of LASP-1. We further demonstrated that LASP-1 was involved in the replication stage of the HCV life cycle. Importantly, LASP-1 expression levels were increased in persistently infected cells with HCV. These data suggest that HCV modulates LASP-1 via NS5A in order to regulate virion levels and maintain a persistent infection.

Current status of hepatitis A virus infections in Korea (한국 소아 A형 간염 현황)

  • Youn, Hee-Shang
    • Clinical and Experimental Pediatrics
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    • v.51 no.7
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    • pp.690-695
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    • 2008
  • The age-specific anti-hepatitis A virus (HAV) seroprevalence rates in South Korea have changed markedly since the last 2030 years with an improvement in the socio-economic, housing, and environmental-sanitation conditions. These changes are characterized by very low anti-HAV seropositive rates among individuals less than 30 years of age; however, nowadays, most adolescents and young adults at an increased risk of developing symptomatic HAV infections. The Korea Center for Disease Control Sentinel Surveillance System has recently revealed an increase in the incidence of hepatitis A infection since 2001 and has revealed a potential endemic nature of the hepatitis A infection. Hepatitis A vaccines that were introduced in 1997 in Korea have made the current anti-HAV IgG positive rates in children (less than 10 years of age) approximately 50% of the rates observed in Seoul in 2006. However, in the same year, a few children were diagnosed as having anti-HAV IgG antibodies in Busan. This suggests the presence of some difference in the vaccination policy among doctors practicing in Seoul and Busan. Thus, the current recommendation of vaccinating 12-year-old child with HAV vaccination should be emphasized and a new strategy should be developed for the vaccination program to cater to the adolescents and young adults who are not immune, as well as for persons who are at a high risk for hepatitis A viral infection such as military personnel and hospital and day care center employees. Further, urgent hepatitis A vaccinations are also needed in patients with chronic liver diseases.

Application of Bovine Viral Diarrhoea Virus as an Internal Control in Nucleic Acid Amplification Tests for Hepatitis C Virus RNA in Plasma-Derived Products

  • Yoo Si Hyung;Hong Seung Hee;Jung Sa Rah;Park Su Jin;Lee Nam Kyung;Kim Soon Nam;Kang Sang Mo;Min Hong Ki;Park Sue Nie;Hong Seung Hwa
    • Journal of Microbiology
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    • v.44 no.1
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    • pp.72-76
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    • 2006
  • Plasma-derived products are produced from plasma via fractionation and chromatography techniques, but can also be produced by other methods. In the performance of nucleic acid amplification tests (NAT) with plasma-derived products, it is necessary to include an internal control for the monitoring of all procedures. In order to avoid false negative results, we confirmed the usefulness of the bovine viral diarrhoea virus (BVDV) for use as an internal control in the detection of hepatitis C virus (HCV) RNA in plasma-derived products. These products, which were spiked with BVDV, were extracted and then NAT was performed. Specificity and sensitivity were determined via the adjustment of primer concentrations and annealing temperatures. BVDV detection allows for validation in the extraction, reverse transcription, and amplification techniques used for HCV detection in plasma-derived products.

Characterization of a Positive Regulatory cis-Element and Transacting Factors for the Hepatitis B Viral Pregenomic Promoter

  • Choi, Cheol-Yong;Park, Geon-Tae;Rho, Hyune-Mo
    • BMB Reports
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    • v.29 no.2
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    • pp.156-162
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    • 1996
  • Transcription of hepatitis B viral pregenomic promoter is known to be regulated mainly by the combined interaction of enhancers I, II and the intervening regulatory sequences between the two enhancers. A positive regulatory element was identified by serial deletion and measuring the linked chloramphenicol acetyltransferase (CAT) activities, which overlapped with the 5' region of the X open reading frame. When the positive regulatory element was inserted upstream of the SV40 early promoter, it elevated SV40 promoter activity in HepG2 cells. Two cellular proteins of 110 (p110) and 33 (p33) kDa interacted with the positive element and both of them were present in the nucleus, but p110 also existed in the cytoplasm in phosphorylated form. Dephosphorylation of p110 by acid phosphatase enhanced the DNA-binding activity of p110. The p33 could bind to single-strand DNA specifically as well as to double-strand DNA.

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A Rapid PCR-based Assay for Detecting Hepatitis B Viral DNA Using GenSpector TMC-1000

  • Huh, Bum;Ha, Young-Ju;Oh, Jae-Tak;Park, Eun-Ha;Park, Jin-Su;Park, Hae-Joon
    • Journal of Applied Biological Chemistry
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    • v.49 no.4
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    • pp.143-147
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    • 2006
  • A rapid PCR-based assay for detecting hepatitis B viral DNA(HBV DNA) in serum and plasma was developed using a new PCR instrument named GenSpector(TMC-1000, Samsung electronics). PCR was carried out using a chip-based platform, which enabled 50 PCR cycles with internal controls, and melting-curve analysis in 30 minutes. Verification of the amplified HBV DNA product and the internal control was based on specific melting temperatures(Tm) analysis, executed by the GenSpector software. Primers were designed within the region conserved through HBV genotypes A to F. The lower limit of detection was 840 copies/ml serum, conducted with serial dilutions of a HBV DNA positive control(ACCURUN 325 series 700, Boston Biomedica Inc.). The assay was also compared to another assay for HBV DNA(Versant HBV DNA 3.0 assay, Bayer HealthCare) for 200 samples(each 100 clinical negative and positive samples). The sensitivity and specificity were 100% matched. This rapid PCR-based assay is specific, reproducible, and enables qualitative detection of HBV DNA.

Hepatitis E Virus Papain-Like Cysteine Protease Inhibits Type I Interferon Induction by Down-Regulating Melanoma Differentiation-Associated Gene 5

  • Kim, Eunha;Myoung, Jinjong
    • Journal of Microbiology and Biotechnology
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    • v.28 no.11
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    • pp.1908-1915
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    • 2018
  • Upon viral infection, the host cell recognizes the invasion through a number of pattern recognition receptors. Melanoma differentiation associated gene 5 (MDA5) and retinoic acid-inducible gene-I (RIG-I) recognize RNA molecules derived from invading viruses, activating down-stream signaling cascades, culminating in the induction of the type I interferon. On the other hand, viruses have evolved to evade type I interferon-mediated inhibition. Hepatitis E virus has been shown to encode a few antagonists of type I interferon and it is not surprising that viruses encode multiple mechanisms of viral evasion. In the present study, we demonstrated that HEV PCP strongly down-regulates MDA5-mediated activation of interferon ${\beta}$ induction in a dose-dependent manner. Interestingly, MDA5 protein expression was almost completely abolished. In addition, polyinosinic polycytidylic acid (poly(I:C))- and Sendai virus-mediated activation of type I interferon responses were similarly abrogated in the presence of HEV PCP. Furthermore, HEV PCP down-regulates several molecules that play critical roles in the induction of type I IFN expression. Taken together, these data collectively suggest that HEV-encoded PCP is a strong antagonist of type I interferon.

Identification of a Cellular Protein Interacting with RNA Polymerase of Hepatitis C Virus

  • Park, Kyu-Jin;Choi, Soo-Ho;Koh, Moon-Soo;Kim, Sung-Wan;Hwang, Soon-Bong
    • BMB Reports
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    • v.33 no.1
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    • pp.59-62
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    • 2000
  • Hepatitis C virus (HCV) nonstructural 5B (NS5B) protein is an RNA-dependent RNA polymerase (RdRp). To determine whether it can contribute to viral replication by interaction with cellular proteins, the yeast two-hybrid screening system was employed to screen a human liver cDNA library. Using the HCV NS5B as a bait, we have isolated positive clones encoding a cellular protein. The NS5B interacting protein, 5BIP, is a novel cellular protein of 170 amino acids. Interaction of the HCV NS5B protein with 5BIP was confirmed by a protein-protein blotting assay. Recently, we have demonstrated that NS5B possesses an RdRp activity and thus it is possible that 5BIP, in association with NS5B, plays a role in HCV replication.

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