Clinical and Molecular Hepatology

"Polymorphism, Single nucleotide"

Editorial

Steatotic liver disease

An analysis of polygenic risk scores for non-alcoholic fatty liver disease: Dae Won Jun; Clin Mol Hepatol 2021;27(3):446-447.
Published online May 21, 2021; DOI: https://doi.org/10.3350/cmh.2021.0133

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Fan Shi, Mei Zhao, Shudan Zheng, Lihong Zheng, Haiqiang Wang
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Fatty liver disease: An updated overview of risk factors
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International journal of health sciences.2023; 7(S1): 3698. CrossRef

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Original Article

Viral hepatitis

No association between the IL28B SNP and response to peginterferon plus ribavirin combination treatment in Korean chronic hepatitis C patients: Nae-Yun Heo, Young-Suk Lim, Woochang Lee, Minkyung Oh, Jiyun An, Danbi Lee, Ju Hyun Shim, Kang Mo Kim, Han Chu Lee, Yung Sang Lee, Dong Jin Suh; Clin Mol Hepatol 2014;20(2):177-184.
Published online June 30, 2014; DOI: https://doi.org/10.3350/cmh.2014.20.2.177

Abstract
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Background/Aims

There are few available data regarding the association between the single nucleotide polymorphisms (SNPs) of the gene encoding interleukin 28B (IL28B) and a sustained virologic response (SVR) to peginterferon (PEG-IFN) plus ribavirin (RBV) therapy in Korean chronic hepatitis C patients.

Methods

This was a retrospective cohort study of 156 patients with chronic hepatitis C virus (HCV) infection who received combination treatment of PEG-IFN plus RBV. Blood samples from these patients were analyzed to identify the IL28B SNPs at rs12979860, rs12980275, rs8099917, and rs8103142. Association analyses were performed to evaluate the relationships between each IL28B SNP and SVRs.

Results

Seventy six patients with HCV genotype 1 and 80 with genotype non-1 were enrolled. The frequencies of rs12979860 CC and CT genotypes were 90.4% and 9.6%, respectively; those of rs12980275 AA and AG genotypes were 87.2% and 12.8%, respectively; those of rs8099917 TT and TG genotypes were 92.3% and 7.7%, respectively; and those of rs8103142 TT and CT genotypes were 90.4% and 9.6%, respectively. Among the patients with HCV genotype 1, the SVR rates were 69.7% and 80.0% for rs12979860 CC and CT, respectively (P=0.71). Among the HCV genotype non-1 patients, SVR rates were 88.0% and 100% for rs12979860 CC and CT (P=1.00), respectively.

Conclusions

Genotypes of the IL28B SNP that are known to be favorable were present in most of the Korean patients with chronic hepatitis C in this study. Moreover, the IL28B SNP did not influence the SVR rate in either the HCV genotype 1 or non-1 patients. Therefore, IL28B SNP analysis might be not useful for the initial assessment, prediction of treatment outcomes, or treatment decision-making of Korean chronic hepatitis C patients.

Citations

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IL28B gene polymorphism rs12979860, but not rs8099917, contributes to the occurrence of chronic HCV infection in Uruguayan patients
Natalia Echeverría, Daniela Chiodi, Pablo López, Adriana Sanchez Ciceron, Jenniffer Angulo, Marcelo López-Lastra, Paola Silvera, Adrian Canavesi, Carla Bianchi, Valentina Colistro, Juan Cristina, Nelia Hernandez, Pilar Moreno
Virology Journal.2018;[Epub] CrossRef
The impact of genetic variation in IL28B, IFNL4 and HLA genes on treatment responses against chronic hepatitis C virus infection
Fatemeh Sakhaee, Morteza Ghazanfari, Farzam Vaziri, Fatemeh Rahimi Jamnani, Mehdi Davari, Safoora Gharibzadeh, Roohollah Fateh, Farid Abdolrahimi, Shahin Pourazar Dizaji, Abolfazl Fateh, Seyed Davar Siadat
Infection, Genetics and Evolution.2017; 54: 330. CrossRef
Immunological dynamics associated with rapid virological response during the early phase of type I interferon therapy in patients with chronic hepatitis C
Jae-Won Lee, Won Kim, Eun-Kyung Kwon, Yuri Kim, Hyun Mu Shin, Dong-Hyun Kim, Chan-Ki Min, Ji-Yeob Choi, Won-Woo Lee, Myung-Sik Choi, Byeong Gwan Kim, Nam-Hyuk Cho, Eui-Cheol Shin
PLOS ONE.2017; 12(6): e0179094. CrossRef
IL28B rs12980275 variant as a predictor of sustained virologic response to pegylated-interferon and ribavirin in chronic hepatitis C patients: A systematic review and meta-analysis
Hao Zheng, Man Li, Bing Chi, Xiao-xue Wu, Jia Wang, Dian-Wu Liu
Clinics and Research in Hepatology and Gastroenterology.2015; 39(5): 576. CrossRef

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Review

Genetic epidemiological study on single nucleotide polymorphisms associated with hepatocellular carcinoma in patients with chronic HBV infection: Yoon Jun Kim , Hyo Suk Lee; Korean J Hepatol 2009;15(1):7-14.
Published online March 31, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.1.7

Abstract
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Hepatocellular carcinoma (HCC) is associated with hepatitis B virus (HBV) as an etiologic agent in 80% of cases, and is the major cause of death among HBV carriers. Family history of HCC is a known risk factor for the development of HCC among chronically HBV infected patients, therefore, genetic factors are likely to modify the risk of HCC. However, the genetic factors that determine progression to HCC remain mostly to be recovered. It is estimated that there are millions of single nucleotide polymorphisms (SNPs) within human genome and they are likely to explain much of the genetic diversity of individuals. In this review, the natural history of HBV infection and host genetic factors related to HCC, study design and target gene selection for the detection of SNPs related to the occurrence of HCC were discussed. Also, several SNPs or haplotypes, which were reportedly associated with increased or reduced risk of HCC occurrence in patients with chronic HBV infection, were reviewed. Especially, recent studies in Korea, one of the HBV endemic areas, were discussed. Screening of these polymorphisms might be useful in clinical practice to stratify the lower or higher risk group for HCC and might modify the design of HCC surveillance programs in patients with chronic HBV infection, if further genetic susceptibilities are identified. The ongoing studies of the distributions and functions of the implicated allele polymorphisms will not only provide insight into the pathogenesis of HCC, but may also provide a novel rationale for new methods of diagnosis and therapeutic strategies. (Korean J Hepatol 2008;15:7-14)

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