Clinical and Molecular Hepatology

"Loss"

Editorial

Viral hepatitis

Old hepatitis B virus never dies: It just hides itself within the host genome: Jeong-Hoon Lee; Clin Mol Hepatol 2021;27(1):107-109.
Published online December 23, 2020; DOI: https://doi.org/10.3350/cmh.2020.0324

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Translational Strategies to Eliminate Chronic Hepatitis B in Children: Prophylaxis and Management in East Asian Countries
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Association of Physical Activity with the Risk of Hepatocellular Carcinoma in Patients with Chronic Hepatitis B
Ho Soo Chun, Sojeong Park, Minjong Lee, Yuri Cho, Ha Sung Kim, A Reum Choe, Hwi Young Kim, Kwon Yoo, Tae Hun Kim
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Original Article

Viral hepatitis

Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers: Kyun-Hwan Kim, Hye-Young Chang, Jun Yong Park, Eun-Sook Park, Yong Kwang Park, Kwang-Hyub Han, Sang Hoon Ahn; Clin Mol Hepatol 2014;20(3):251-260.
Published online September 25, 2014; DOI: https://doi.org/10.3350/cmh.2014.20.3.251

Abstract
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Background/Aims

Occult HBV infection can persist following HBsAg loss and be transmitted, but the virological features are not well defined.

Methods

Here we investigated 25 Korean patients who lost HBsAg during follow up, either spontaneously or subsequent to therapy.

Results

Whereas subtype adr (genotype C) was found in 96% of HBsAg positive patients, 75 % of patients who lost HBsAg spontaneously were seemed to be infected with the ayw subtype with sequence similar to genotype D. Mutations in the major hydrophilic region (MHR) of HBsAg were found in 7 patients who lost HBsAg spontaneously. The mutations include T123S, M125I/N, C139R, D144E, V177A, L192F, and W196L, some of which have not been reported before. Functional analysis via transfection experiments indicate that the C139R and D144E mutations drastically reduced HBsAg antigenicity, while the Y225del mutation found in one interferon-treated patient impaired HBsAg secretion.

Conclusions

Lack of detectable HBsAg in patient serum could be explained by low level of ccc DNA in liver tissue, low antigenicity of the surface protein, or its secretion defect.

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mBio.2025;[Epub] CrossRef
Evolution and diversity of the hepatitis B virus genome: Clinical implications
Chengzuo Xie, Daiqiang Lu
Virology.2024; 598: 110197. CrossRef
Role of S protein transmembrane domain mutations in the development of occult hepatitis B virus infection
Xinyi Jiang, Le Chang, Ying Yan, Huimin Ji, Huizhen Sun, Yingzi Xiao, Shi Song, Kaihao Feng, Abudulimutailipu Nuermaimaiti, Lunan Wang
Emerging Microbes & Infections.2022; 11(1): 2184. CrossRef
Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection
Hao Wang, Min Wang, Jieting Huang, Ru Xu, Qiao Liao, Zhengang Shan, Yourong Zheng, Xia Rong, Xi Tang, Tingting Li, Wenjing Wang, Chengyao Li, Yongshui Fu
Journal of Viral Hepatitis.2020; 27(9): 915. CrossRef
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Yu. O. Ostankova, A. V. Semenov, E. B. Zueva, A. A. Totolian
HIV Infection and Immunosuppressive Disorders.2019; 11(1): 64. CrossRef
Investigation of a Novel Hepatitis B Virus Surface Antigen (HBsAg) Escape Mutant Affecting Immunogenicity
Md. Golzar Hossain, Keiji Ueda, Isabelle A Chemin
PLOS ONE.2017; 12(1): e0167871. CrossRef
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PLOS ONE.2017; 12(5): e0172101. CrossRef
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Zhenhua Zhang, Ling Zhang, Yu Dai, Yafei Zhang, Jun Li, Xu Li
Virology Journal.2016;[Epub] CrossRef
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Hui-Lan Zhu, Xu Li, Jun Li, Zhen-Hua Zhang
World Journal of Gastroenterology.2016; 22(13): 3531. CrossRef
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Journal of microbiology, epidemiology and immunobiology.2016; 93(5): 34. CrossRef
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Case Report

A case of sudden-onset hearing Loss in a patient treated with peginterferon α-2b and ribavirin for chronic hepatitis C: Min Ki Shin , Tae Hyo Kim , Kang Ju , Chang Yoon Ha , Hyun Ju Min , Woon Tae Jung , Ok Jae Lee; Korean J Hepatol 2009;15(3):370-374.
Published online September 30, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.3.370

Abstract
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Combination therapy of pegylated interferon α and ribavirin has been associated with various adverse effects, but sudden-onset hearing loss is uncommon. We report a 60-year-old male patient who developed sudden-onset hearing loss during combination therapy with pegylated interferon α and ribavirin for chronic hepatitis C. This patient had been diagnosed with chronic hepatitis C (genotype Ib) and early-stage liver cirrhosis 3 years previously, and had been treated with conventional interferon-α and ribavirin for 12 months. However, 6 months from the end of the treatment course the patient relapsed and received combination retreatment with pegylated interferon α-2b and ribavirin. He developed sudden-onset right-side hearing loss and tinnitus 42 weeks after the start of this retreatment. Pure-tone audiometry revealed a right-side hearing loss of 60~90dB. The patient consequently immediately discontinued the pegylated interferon therapy and was given prednisone 60 mg/day for 10 days, after which the hearing loss had almost completely recovered. (Korean J Hepatol 2009;15:370-374)

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Unilateral hearing loss due to pegylated interferon-α2b and ribavirin therapy
Savita Jain, Vandana Midha, Ajit Sood
Indian Journal of Gastroenterology.2011; 30(5): 239. CrossRef

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Original Articles

Change of HBV DNA Level as a Predictor of HBeAg Loss after Lamivudine Treatment: Jae Kwon Jung, M.D., Chang Hyeong Lee, M.D., Eun Young Kim, M.D., Jin Tae Jung, M.D., Joon Hyuck Choi, M.D., Ji Min Han, M.D., Myoung In Jin, M.D., Ju Yeon Cho, M.D., Byung Seok Kim, M.D., Im Hee Shin, Ph.D.1; Korean J Hepatol 2007;13(4):513-520.
Published online December 20, 2007; DOI: https://doi.org/10.3350/kjhep.2007.13.4.513

Abstract
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Backgroud/Aims: Lamivudine is an effective, safe therapeutic agent for the treatment of chronic hepatitis B. The aim of this study was to investigate whether early suppression of the viral load predicts HBeAg loss within 1 year during lamivudine therapy. Methods: This prospective study encompassed 74 patients (mean age: 37.1 years, male/female: 51/23) who were positive HBeAg, their AST or ALT levels were ≥2 times the upper limit of normal and their HBV DNA was ≥105 copies/mL. The patients received lamivudine 100 mg for 12 months with monitoring their HBV DNA, AST, ALT, HBeAg and anti-HBe, and all these tests were performed at pretreatment and 1, 3, 6, 9 and 12 months after treatment. The serum HBV DNA was measured by HBV branched DNA assay. Results: HBeAg loss was observed in 12 patients (16.2%), and 9 patients achieved anti-HBe seroconversion during up to 1 year of lamivudine therapy. The mean time to HBeAg loss was 5.6 months (range: 1-12 months). The posttreatment HBV DNA (<2,000 copies/mL) after 3 month (P=0.008) and 6 month (P=0.012)) were significant predictors of HBeAg loss after 1 year of lamivudine treatment on univariate analysis. Pretreatment HBV DNA, AST/ALT, gender, age and liver cirrhosis had no impact on HBeAg loss. The six-month posttreatment HBV DNA level <2,000 copies/mL was a significant predictor of HBeAg loss on multivariate analysis (P=0.008, odds ratio=0.108). Conclusion: We suggest that an HBV DNA level <2,000 copies/mL at 6 month after lamivudine therapy is the most important predictor of HBeAg loss during up to 1 year of lamivudine therapy. (Korean J Hepatol 2007;13:513-520)

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Loss of Heterozygosity of p73, APC, and p53 in Hepatoblastoma: Han Seong Kim,Young Mi Jung,Mi Ran Kim,Jung Young Lee,Mi Sook Lee,Ja June Jang; Korean J Hepatol 1999;5(1):43-49.

Abstract
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Background/Aims
: The status of tumor suppression gene can be assessed indirectly by analyzing the loss of heterozygosity. Hepatoblastoma is a malignant liver tumor in childhood. To find the molecular carcinogenetic mechanism of hepatoblastoma, loss of heterozygosity (LOH) of p73, APC and p53 was studied. Materials and
methods
: Hepatoblastoma tissues from thirty- three cases were collected by lobectomy or tumorectomy. On H- E stained sections, normal and tumor cells were microdissected separately and LOH analysis was perfomed using 8 markers: six of p73, one of APC and one of p53. Results : Number of cases showing at least one LOH in six p73 markers was four out of twenty- six (15.4%): each LOH frequencies in D1S160, D1S170, D1S199, D1S228, D1S243 and D1S253 were in order of 7.7%, 0%, 9.1%, 0%, 12.5% and 0%. LOH frequency of APC was 41.7% and that of p53 was 13.3%. Conclus ion : Low LOH frequency of p73 related markers indicates that p73 gene may not be implicated in carcinogenesis of hepatoblastoma. (Korean J Hepatol 1999;5:43－49)

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Pretreatment ALT Level and Histologic Activity as Predictors of HBeAg Loss in Lamivudine Treatment for Chronic Hepatitis B: Young Oh Kweon, M.D. and Kyung Hee Kang, M.D.; Korean J Hepatol 2004;10(1):31-41.

Abstract
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Background/Aims
Lamivudine is a potent inhibitor of hepatitis B virus replication, but an increased incidence of YMDD mutation may be associated with its long term use. Thus, the decision to initiate therapy should be based on variables that are predictive of lamivudine-induced HBeAg loss. The objective of this analysis was to determine patient-dependent or laboratory variables that predict HBeAg loss. Methods: We retrospectively analyzed 99 HBeAg-positive patients with chronic hepatitis B who were treated with lamivudine and followed up for more than 52 weeks. All patients had a liver biopsy before starting lamivudine therapy. HBeAg loss and HBeAg seroconversion after 52 weeks of treatment were defined as endpoints. Results: The overall rates of HBeAg loss and HBeAg seroconversion were 41.4% (41/99) and 37.4% (37/99), respectively. The rates of HBeAg loss increased as pretreatment ALT levels increased (P=0.013) and were highest among patients with pretreatment ALT levels greater than 5 times the upper limit of normal, occurring in 56.8% of those patients. The rate of HBeAg loss was higher in patients with more active histologic disease on pretreatment liver biopsy (Grade 1&2 vs. Grade 3&4, 28.3% vs 56.5%, P=0.004). Similar results were seen with HBeAg seroconversion, though seroconversion occurred less frequently than HBeAg loss. Multivariate analysis showed that elevated baseline ALT levels (P<0.05) and histologic activity (P<0.05) were the best independent predictors of HBeAg loss and seroconversion in response to lamivudine. Conclusions: Pretreatment ALT levels and histologic activity were the most important predictors for response to lamivudine.(Korean J Hepatol 2002;10:31-41)