Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication

Li, Changzheng; Kato, Naoya; Chang, Jin-Hai; Muroyama, Ryosuke; Shao, Run–Xuan; Dharel, Narayan; Sermsathanasawadi, Radsamee; Kawabe, Takao; Omata, Masao

doi:10.1111/j.1478-3231.2009.02061.x

Cited by 23 publications

(23 citation statements)

References 42 publications

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“…Variants in MYL2 and C12orf51 also showed strong association with HDLc in this study. OAS1, encoding an enzyme of the innate immune system, has an antiviral function 6 . It has been reported that polymorphisms of OAS1 are involved in the progression of disease after hepatitis C virus infection 6 l e t t e r s 0.0008).…”

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confidence: 99%

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Large-scale genome-wide association studies in east Asians identify new genetic loci influencing metabolic traits

et al. 2011

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l e t t e r sTo identify the genetic bases for nine metabolic traits, we conducted a meta-analysis combining Korean genome-wide association results from the KARE project (n = 8,842) and the HEXA shared control study (n = 3,703). We verified the associations of the loci selected from the discovery metaanalysis in the replication stage (30,395 individuals from the BioBank Japan genome-wide association study and individuals comprising the Health2 and Shanghai Jiao Tong University Diabetes cohorts). We identified ten genome-wide significant signals newly associated with traits from an overall metaanalysis. The most compelling associations involved 12q24.11 (near MYL2) and 12q24.13 (in C12orf51) for high-density lipoprotein cholesterol, 2p21 (near SIX2-SIX3) for fasting plasma glucose, 19q13.33 (in RPS11) and 6q22.33 (in RSPO3) for renal traits, and 12q24.11 (near MYL2), 12q24.13 (in C12orf51 and near OAS1), 4q31.22 (in ZNF827) and 7q11.23 (near TBL2-BCL7B) for hepatic traits. These findings highlight previously unknown biological pathways for metabolic traits investigated in this study.

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“…OAS1, encoding an enzyme of the innate immune system, has an antiviral function 6 . It has been reported that polymorphisms of OAS1 are involved in the progression of disease after hepatitis C virus infection 6 l e t t e r s 0.0008). The protein encoded by ZNF827 may be a transcriptional regulator that affects plasma GGT levels.…”

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Large-scale genome-wide association studies in east Asians identify new genetic loci influencing metabolic traits

et al. 2011

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“…Several biomarkers have recently been evaluated in the context of HCV infection, including interferon-responsive genes (26,30,37,40,51,53), chemokines (28,29,31,54,56), interleukin-28B (IL-28B) gene polymorphisms (16,18,39), fibrosis protein markers (6,7,35), fibrinogen-like protein 2 (11), complement component C3a (25), and osteopontin (23).…”

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confidence: 99%

Danoprevir Monotherapy Decreases Inflammatory Markers in Patients with Chronic Hepatitis C Virus Infection

Schaefer¹,

Kossen²,

Lim³

et al. 2011

Antimicrob Agents Chemother

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Danoprevir is a potent and selective direct-acting antiviral agent that targets the protease activity of hepatitis C virus (HCV) NS3/4A. This agent results in a significant rapid decline in HCV RNA levels when it is used in monotherapy. The present study evaluated whether plasma concentrations of the inflammatory markers gamma interferon-inducible protein 10 (IP-10) and neopterin or the interferon-stimulated gene product 2-5-oligoadenylate synthetase (OAS-1) were correlated with the plasma HCV RNA concentration before or during 14-day danoprevir monotherapy. In contrast to pegylated interferon and ribavirin treatment, a higher baseline IP-10 concentration was positively correlated with a greater first-phase HCV RNA decline upon danoprevir administration. Changes in the IP-10 plasma concentration during danoprevir administration were also associated with categorical changes in HCV RNA concentration at days 7 and 14. The neopterin concentration appeared to be moderately decreased during danoprevir administration, although these changes were not statistically significant. However, changes in neopterin concentration showed a statistically significant correlation with changes in IP-10 concentration. Considerable variation in the OAS-1 concentration was observed before and during treatment, including in patients treated with placebo and/or patients with minimal virologic response. Overall, these results suggest that effective treatment with a direct-acting antiviral agent may reduce hepatic inflammation and that first-phase HCV RNA decline during treatment with an NS3/4A protease inhibitor is more robust in patients with high baseline IP-10 concentrations.

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“…(37)(38)(39) Gene polymorphisms associated with activity of hepatitis and liver fibrosis progression, which contribute to the development of HCC, have also been reported in HCV patients. (40,41) In spite of this effort, most studies had insufficient sample sizes, and the associations with HCV-related HCC were not robust. Therefore, better predictive genetic markers are still needed.…”

Section: Epidemiology and Risk Factors Of Hccmentioning

confidence: 99%

Hepatocellular carcinoma: Towards personalized medicine

et al. 2012

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Over the past several years, the success of genome-wide association studies (GWAS) and pharmacogenomics has gradually begun to enable personalized medicine in some fields. In the field of liver diseases, host genetic factors are now very useful in clinical practice for predicting treatment outcome and adverse reactions for pegylated interferon plus ribavirin combination therapy against chronic hepatitis C virus (HCV) infection. Recently, three virus-related hepatocellular carcinoma (HCC) GWAS were reported from Asia. One study examined hepatitis B virus-related HCC in China, where hepatitis B is very prevalent, and the other two examined HCV-related HCC in Japan. We identified a common variant in the DEPDC5 locus associated with HCV-related HCC, and another group identified an association involving the MICA locus. In this review, we compare the results of these GWAS and earlier candidate gene studies. Further research is needed to determine the role of these single nucleotide polymorphisms on HCC risk, but identification of these markers could make it possible to assess the magnitude of the risk of cancer based on each patient's genetic background. Consideration of the genetic background of the patients will likely play a role in personalized medicine for HCC, and understanding the mechanism underlying the association could suggest novel promising therapeutic targets in the future. (Cancer Sci 2012; 103: 846-850) O ver the last several years, the success of GWAS and the International HapMap Project, a large-scale database of SNPs, has identified genetic risk factors for more than 150 diseases, as well as genetic differences in drug response.(1-4) The success of these studies as well as pharmacogenomics has gradually begun to enable personalized medicine in some fields. (5)(6)(7)(8) The goal of personalized medicine is to optimize the medical care and outcomes for each patient based on clinical, genetic, and environmental information.(9) In the field of liver diseases, host genetic factors are now very useful in clinical practice for predicting treatment outcome and adverse reactions of PEG-IFN-a plus ribavirin combination therapy against chronic HCV infection, (10)(11)(12)(13)(14)(15)(16)(17) which causes chronic hepatitis and HCC. Epidemiology and Risk Factors of HCCHepatocellular carcinoma is the third leading cancer-related cause of death and the seventh most common form of cancer worldwide. (18) There are 750 000 new cases of HCC and nearly 700 000 deaths each year, making it a lethal form of cancer. (18) A variety of risk factors for HCC have been reported, including hepatitis viruses, vinyl chloride, tobacco, aflatoxin B1, alcohol consumption, non-alcoholic fatty liver disease, diabetes mellitus, obesity, diet, coffee, oral contraceptives, and hemochromatosis.(19) Incidence of HCC varies around the world, largely reflecting the distribution of HBV and HCV. As HBV infection is highly prevalent in many Asian countries and in Africa, HBV is the most common etiology of HCC in these regions, whereas in many ...

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Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication

Abstract: The SNP of OAS-1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.

Cited by 23 publications

References 42 publications

Large-scale genome-wide association studies in east Asians identify new genetic loci influencing metabolic traits

Large-scale genome-wide association studies in east Asians identify new genetic loci influencing metabolic traits

Danoprevir Monotherapy Decreases Inflammatory Markers in Patients with Chronic Hepatitis C Virus Infection

Hepatocellular carcinoma: Towards personalized medicine

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