کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2823353 | 1161383 | 2009 | 6 صفحه PDF | دانلود رایگان |
Low-density lipoprotein receptor (LDLR) is involved in the entry of hepatitis C virus (HCV) in host cells. We investigated whether three single-nucleotide alterations within LDLR might be associated with the course of hepatitis C infection and response to antiviral therapy. We enrolled 651 individuals with chronic HCV infection who had received interferon-based combination therapy, 174 individuals with self-limited HCV infection, and 516 healthy controls. LDLR c.1171G > A, c.1413G > A, and c.*52G > A genotyping was performed by real-time PCR-based assays. HCV genotype 1-infected individuals who were homozygous for 3′UTR c.*52G were at increased risk for virologic non-response to antiviral therapy compared to virologic responders (66.3% vs. 51.0%, p = 0.001). Furthermore, compared to healthy controls, self-limited HCV genotype 1 infection was significantly associated with c.1171A (15.1% vs. 6.6%, p = 0.006) and negatively associated with c.1413G > A heterozygosity (33.0% vs. 46.1%, p = 0.023). The data indicate that LDLR alterations are correlated with response to interferon-based combination therapy and with self-limitation of HCV 1 infection.
Journal: Infection, Genetics and Evolution - Volume 9, Issue 5, September 2009, Pages 847–852