title: Association of Toll-Like Receptor 3 Single-Nucleotide Polymorphisms and Hepatitis C Virus Infection.
abstract: Toll-like receptor 3 (TLR3) plays a key role in innate immunity by recognizing pathogenic, double-stranded RNAs. Thus, activation of TLR3 is a major factor in antiviral defense and tumor eradication. Although downregulation ofTLR3gene expression has been mainly reported in patients infected with hepatitis C virus (HCV), the influence of TLR3 genotype on the risk of HCV infection, HCV-related cirrhosis, and/or hepatocellular carcinoma (HCC) remains to be determined. Single-nucleotide polymorphisms (SNPs) within theTLR3gene and their associations with HCV-related disease risk were investigated in a Saudi Arabian population in this study. EightTLR3SNPs were analyzed in 563 patients with HCV, which consisted of 437 patients with chronic HCV infections, 88 with HCV-induced liver cirrhosis, and 38 with HCC. A total of 599 healthy control subjects were recruited to the study. Among the eightTLR3SNPs studied, the rs78726532 SNP was strongly associated with HCV infection when compared to that in healthy control subjects. The rs5743314 was also strongly associated with HCV-related liver disease progression (cirrhosis and HCC). In summary, these results indicate that distinct genetic variants ofTLR3SNPs are associated with HCV infection and HCV-mediated liver disease progression in the Saudi Arabian population.
authors.affiliation: Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
authors.forename: Mashael R
authors.initials: MR
authors.lastname: Al-Anazi
authors.affiliation: Cell and Gene Therapy Group, Medical Genomics Research Department, King Abdullah International Medical Research Center, Ministry of National Guard, Riyadh, Saudi Arabia.
authors.forename: Sabine
authors.initials: S
authors.lastname: Matou-Nasri
authors.affiliation: Section of Gastroenterology, Department of Medicine, College of Medicine, King Saud University, Riyadh, Saudi Arabia; Liver Disease Research Center, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Ayman A
authors.initials: AA
authors.lastname: Abdo
authors.affiliation: Liver Disease Research Center, King Saud University, Riyadh, Saudi Arabia; Gastroenterology Unit, Department of Medicine, King Abdulaziz Medical City, Jeddah, Saudi Arabia.
authors.forename: Faisal M
authors.initials: FM
authors.lastname: Sanai
authors.affiliation: Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Saad
authors.initials: S
authors.lastname: Alkahtani
authors.affiliation: Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Saud
authors.initials: S
authors.lastname: Alarifi
authors.affiliation: Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Abdullah A
authors.initials: AA
authors.lastname: Alkahtane
authors.affiliation: Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Hamad
authors.initials: H
authors.lastname: Al-Yahya
authors.affiliation: Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Daoud
authors.initials: D
authors.lastname: Ali
authors.affiliation: Department of Biology, Science College, AI-Imam Muhammad Ibn Saud Islamic University, Riyadh, Saudi Arabia.
authors.forename: Mohammed S
authors.initials: MS
authors.lastname: Alessia
authors.affiliation: Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
authors.forename: Bushra
authors.initials: B
authors.lastname: Alshahrani
authors.affiliation: Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia; Department of Microbiology and Immunology, Alfaisal University School of Medicine, Riyadh, Saudi Arabia.
authors.forename: Mohammed N
authors.initials: MN
authors.lastname: Al-Ahdal
authors.affiliation: Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia; Department of Microbiology and Immunology, Alfaisal University School of Medicine, Riyadh, Saudi Arabia.
authors.forename: Ahmed A
authors.identifier: 0000-0003-4584-5739
authors.initials: AA
authors.lastname: Al-Qahtani
mesh_terms: D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000209:etiology / Q000235:genetics*; D005260:Female; D005355:Fibrosis / Q000209:etiology / Q000235:genetics*; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000150:complications / Q000235:genetics*; D006801:Humans; D008113:Liver Neoplasms / Q000209:etiology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012306:Risk; D012529:Saudi Arabia; D051196:Toll-Like Receptor 3 / Q000235:genetics*; D055815:Young Adult
chemical_list: C495344:TLR3 protein, human; D051196:Toll-Like Receptor 3