title: Genetic polymorphism of low-density lipoprotein receptor did not affect treatment outcome of chronic hepatitis C genotype 3.
abstract: 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.
  
  
  METHODS
  A total of 112 naïve 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 HCVRNA viral load and alanine aminotransferase level were 6.3 log, 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.
  
  
  CONCLUSIONS
  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
authors: Division of Gastroenterology, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Bangkok, Thailand. sittw@mahidol.ac.th
authors: Tawesak
authors: T
authors: Tanwandee
authors: Manop
authors: M
authors: Pithukpakorn
authors: Noppawan
authors: N
authors: Vipatakul
authors: Phunchai
authors: P
authors: Charatcharoenwitthaya
authors: Siwaporn
authors: S
authors: Chainuvati
authors: Supot
authors: S
authors: Nimanong
authors: Varayu
authors: V
authors: Prachayakul
authors: Supot
authors: S
authors: Pongprasobchai
authors: Sathaporn
authors: S
authors: Manatsathit
authors: Somchai
authors: S
authors: Leelakusolvong
authors: Nonthalee
authors: N
authors: Pausawasdi
authors: Udom
authors: U
authors: Kachintorn
authors: Chanin
authors: C
authors: Limwongse
authors: Suthipol
authors: S
authors: Udompunturak
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000410:Alanine Transaminase / Q000235:genetics / Q000378:metabolism; D000998:Antiviral Agents / Q000627:therapeutic use*; D002908:Chronic Disease; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000235:genetics* / Q000821:virology; D006801:Humans; D007372:Interferons / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D012367:RNA, Viral / Q000235:genetics; D011973:Receptors, LDL / Q000235:genetics*; D012254:Ribavirin / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D012367:RNA, Viral; D011973:Receptors, LDL; D012254:Ribavirin; D007372:Interferons; D000410:Alanine Transaminase