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Impact Of Host Il28 B Rs12979860, Rs8099917 In Interferon Responsiveness And Advanced Liver Disease In Chronic Genotype 3 Hepatitis C Patients

1663 words - 7 pages

Chronic hepatitis C virus (HCV) infection is a major cause for developing cirrhosis and hepatocellular carcinoma (HCC), with an estimated global prevalence of 3% occurring in about 180 million carriers and more than 350,000 people die every year from hepatitis C-related liver diseases [1, 2]. According to World Health Organization reports, HCV is found worldwide with certain countries having chronic infection rates as high as 5% or above. In India 12.5 million people are infected with HCV [2]. This virus is spread primarily by blood to blood contact associated with intravenous drug use, poorly sterilized medical equipment and improper transfusions [3]. Hepatitis C virus (HCV) is a small ...view middle of the document...

But till now, an increased incidence of HCC in cirrhotic patients infected with genotype 3 has not been documented. The gold standard therapy for chronic hepatitis C (CHC) consists of pegylated interferon (Peg-IFN) and ribavirin, but reports have shown the drugs are not well tolerated [8]. Therefore, it is the need of the hour to identify determinants of response of treatment. Recent observations on the genetic determinants of CHC established that a single nucleotide polymorphism (SNP) in the interleukin (IL)-28B gene influences the treatment outcome of the HCV. IL28B gene encodes IFN-λ3, a cytokine, distantly related to type I IFNs and the interleukin (IL)-10 family. Together with IL28A (IFN-λ2) and IL29 (IFN-λ1), IL28B forms a cytokine gene cluster on a chromosomal region mapped to 19q13. Expression of the cytokines encoded by these three genes can be induced by ribonucleic acid (RNA) virus infection [8]. Studies have also shown that IL28B gene expression can inhibit HCV replication through Janus Kinase signal transducer and activator of transcription pathway in time and dose dependent manner [9]. In September 2009, Ge et al. [10] in a genome-wide association study (GWAS) found the rs12979860 single nucleotide polymorphism (SNP), which is located 3 kb upstream of the IL28B gene, to be the strongest host genetic predictor of SVR in hepatitis C genotype 1. They observed that rs12979860 CC patients, regardless of their ethnicity, reach Sustained Virological Response (SVR) rates approximately twice that of rs12979860 TT patients. The researchers also found that the highest percentage of favorable allele amongst Asians and lowest amongst Africans which in part explains the high rate of favorable response to interferon (IFN) in Asians as compared to Africans. Another GWAS study in 2009 by Suppiah and Tanaka et al found that an additional polymorphism at rs80999917 which is located around 8kb upstream of the IL28B to be a strong genetic determinant of SVR in HCV genotype 1 infected patients [11, 12]
Different studies have shown that race, genotype, HCV RNA viral load, age, gender, basal metabolic index (BMI), fibrosis are important predictors for information regarding the IFN –ribavirin (IFN/RBV) treatment response [7]. The impact of IL28B associations in interferon responsiveness amongst Indian population remains understudied. In the current era, new HCV treatment paradigm includes one direct acting antiviral (DAA), a protease inhibitor (PI), in combination with Peg-IFN and ribavirin. The addition of DAA to Peg-IFN/RBV nearly doubles the chances of response to treatment but at the cost of increased toxicity [13]. These drugs have shown significant increase in SVR rates but the problem remains in the developing countries like India, where the DAA is still not introduced and if commenced; initial costs might be high for the people to afford the expensive treatment. Thus, in these clinical settings; IL28B genotyping in predicting IFN responsiveness...

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