Abstract
Host genetic factors may predict the outcome and treatment response in hepatitis C virus (HCV) infection. One of these factors is the single nucleotide polymorphisms of the interleukin 28B (IL28B) gene. We sought to evaluate the outcome of pegylated interferon and ribavirin therapy in association with IL-28B rs8099917 and rs12980275 in patients infected with HCV genotype 4. A total of 180 patients with chronic hepatitis C were selected from Egyptians who have received combined therapy with pegylated interferon and ribavirin for 6 months and their response was evaluated after follow-up at 0, 6, 12, 24 and 48 weeks from the beginning of the therapy. Blood samples were collected from responders and non-responders. Genomic DNA was extracted from whole blood and genotyping was carried out by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Our results showed that TT genotype of rs8099917 was associated with higher sustained viral response (SVR) rates and G allele represented a risk factor for failure of response (OR = 3.7, CI = 1.8:7.64) while rs12980275 was not significantly associated with SVR in genotype 4 Egyptian patients. The determination of IL-28B SNPs may be useful in enhancing correct prediction of SVR achievement in treating this group of genotype 4 patients.
Highlights
Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide[1]
Recent genome-wide association studies (GWAS) have shown that human genetic variations of the gene for interleukin 28B (IL-28B) may explain differences in treatment outcomes of adults chronically infected with HCV and that they can be useful as therapy response markers[8,9,10,11]
In responders and 33.33% in non-responders while the frequency of "TG type of rs8099917" and GG type was 20% among responders and 66.67% in patients who did not respond to combined treatment showing a significant difference in these polymorphisms (P50.001, Table 2) with (OR58; 95%CI54.0615.7, P50.001) (Table 3)
Summary
Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide[1]. There are 7 major HCV genotypes, which have different geographical distributions and susceptibilities to interferon-a treatment[2]. The combination of pegylated interferon and ribavirin is still the most effective therapy in HCV-4[4], and the success rate of current therapy chronic hepatitis C is related to a variety of host and viral factors that can be used as response predictors[5,6]. Recent genome-wide association studies (GWAS) have shown that human genetic variations (single-nucleotide polymorphisms, SNPs) of the gene for interleukin 28B (IL-28B) may explain differences in treatment outcomes of adults chronically infected with HCV and that they can be useful as therapy response markers[8,9,10,11].
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