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Original ArticleOpen Access
Genetic Polymorphism of Low-Density Lipoprotein Receptor Did Not Affect Treatment Outcome of Chronic Hepatitis C Genotype 3
Tanwandee T 
,
Pithukpakorn M ,
Vipatakul N ,
Charatcharoenwitthaya P ,
Chainuvati S ,
Nimanong S ,
Prachayakul V ,
Pongprasobchai S ,
Manatsathit S ,
Leelakusolvong S ,
Pausawasdi N ,
Kachintorn U ,
Limwongse C ,
Udompunturak S
,
Pithukpakorn M ,
Vipatakul N ,
Charatcharoenwitthaya P ,
Chainuvati S ,
Nimanong S ,
Prachayakul V ,
Pongprasobchai S ,
Manatsathit S ,
Leelakusolvong S ,
Pausawasdi N ,
Kachintorn U ,
Limwongse C ,
Udompunturak S Background: The low-density lipoprotein receptor (LDL-R) has been proposed to function as a receptor for the hepatitis C
virus (HCV) entry. Polymorphism of LDL-R gene may influence the clearance of virus and response to treatment. This study
was conducted to evaluate the association of LDL-R gene polymorphism and the response to antiviral treatment in patients
with chronic HCV infection.
Material and Method: A total of 112 nave patients with HCV genotype 3 were enrolled in the study. All patients were treated
with a combination of pegylated interferon and ribavirin for 24 weeks. Polymerase chain reaction combined with restriction
fragment length polymorphism was used to detect the polymorphism at the LDL-R gene intron 11 loci, including intron1,
intron 3.1, intron 3.2, intron 4, intron 6, exon 8, intron 11, intron 13, intron 14 and 3’UTR-2 SNPs in intron 16 region.
Comparisons of genotype and allele frequency between responders and nonresponders were analyzed.
Results: Patients had a mean age of 54 years and 43% were male. Mean HCV RNA viral load and alanine aminotransferase
level were 6.3 log10 IU/mL and 100 IU/L, respectively. Sustained virological response, relapse and no response were
documented in 68.7%, 17.9% and 13.4%, respectively. Baseline characteristics including age, sex, body weight,
aminotransferase levels and HCV RNA viral load were similar between responders and nonresponders. No statistical
difference was found for either genotype distribution or allele frequency among responders and nonresponders.
Conclusion: This study did not provide the evidence for a role of LDL-R polymorphism the response to antiviral treatment
in patients with HCV genotype 3. This indicates that a genetic component via the LDL-R may not control HCV treatment
outcome in HCV genotype 3
Keywords: Hepatitis C virus, Low-density lipoprotein receptor, Low-density lipoprotein receptor polymorphism, Hepatitis C
virus treatment response
virus (HCV) entry. Polymorphism of LDL-R gene may influence the clearance of virus and response to treatment. This study
was conducted to evaluate the association of LDL-R gene polymorphism and the response to antiviral treatment in patients
with chronic HCV infection.
Material and Method: A total of 112 nave patients with HCV genotype 3 were enrolled in the study. All patients were treated
with a combination of pegylated interferon and ribavirin for 24 weeks. Polymerase chain reaction combined with restriction
fragment length polymorphism was used to detect the polymorphism at the LDL-R gene intron 11 loci, including intron1,
intron 3.1, intron 3.2, intron 4, intron 6, exon 8, intron 11, intron 13, intron 14 and 3’UTR-2 SNPs in intron 16 region.
Comparisons of genotype and allele frequency between responders and nonresponders were analyzed.
Results: Patients had a mean age of 54 years and 43% were male. Mean HCV RNA viral load and alanine aminotransferase
level were 6.3 log10 IU/mL and 100 IU/L, respectively. Sustained virological response, relapse and no response were
documented in 68.7%, 17.9% and 13.4%, respectively. Baseline characteristics including age, sex, body weight,
aminotransferase levels and HCV RNA viral load were similar between responders and nonresponders. No statistical
difference was found for either genotype distribution or allele frequency among responders and nonresponders.
Conclusion: This study did not provide the evidence for a role of LDL-R polymorphism the response to antiviral treatment
in patients with HCV genotype 3. This indicates that a genetic component via the LDL-R may not control HCV treatment
outcome in HCV genotype 3
Keywords: Hepatitis C virus, Low-density lipoprotein receptor, Low-density lipoprotein receptor polymorphism, Hepatitis C
virus treatment response
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