title: Polymorphism of tumor necrosis factor-α and interleukin-10 gene promoter region in chronic hepatitis C virus patients and their effect on pegylated interferon-α therapy response.
abstract: The development and resolution of an inflammatory process is regulated by a complex interplay among cytokines that have pro- and anti-inflammatory effects. Regulatory mechanisms that control the production of cytokines include genetic polymorphism in particular promoter/leader region. Polymorphisms may directly or indirectly affect the binding of transcriptional factors, consequently increasing or decreasing the production of mRNA, thus regulating cytokine production. A total of 70 hepatitis C virus (HCV) RNA-positive patients and 70 healthy control subjects were included in the present study, who were attending the medical outpatient department (OPD) and wards of a tertiary care hospital in New Delhi during 2006-2008. This study was designed to determine the polymorphism of tumor necrosis factor-α and interleukin-10 genes in patients with chronic HCV infection patients and their effect on pegylated interferon-α therapy response. Polymorphism in the tumor necrosis factor-α G/G, G/A, and A/A genotype was significant between HCV patients and healthy controls. Interleukin-10 variants (G/G, G/A) were nonsignificant among HCV patients compared with healthy controls. As this is a preliminary study on small sample size, we believe that our findings may stimulate further studies on larger number of patients from this geographic region.
authors.affiliation: Department of Microbiology, Maulana Azad Medical College & Associated Lok Nayak Hospital, New Delhi, India.
authors.forename: Gaurav
authors.initials: G
authors.lastname: Dogra
authors.forename: Anita
authors.initials: A
authors.lastname: Chakravarti
authors.forename: Premashish
authors.initials: P
authors.lastname: Kar
authors.forename: Yogesh Kumar
authors.initials: YK
authors.lastname: Chawla
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000008:administration & dosage / Q000627:therapeutic use; D054316:Biomarkers, Pharmacological / Q000097:blood; D016022:Case-Control Studies; D005838:Genotype; D016174:Hepacivirus / Q000502:physiology*; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology / Q000235:genetics*; D006801:Humans; D007194:India; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage* / Q000627:therapeutic use; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics*; D008875:Middle Aged; D010045:Outpatients; D011092:Polyethylene Glycols / Q000008:administration & dosage* / Q000627:therapeutic use; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000627:therapeutic use; D012254:Ribavirin / Q000008:administration & dosage / Q000627:therapeutic use; D017422:Sequence Analysis, DNA; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics*
chemical_list: D000998:Antiviral Agents; D054316:Biomarkers, Pharmacological; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D011092:Polyethylene Glycols; D012254:Ribavirin; C417083:peginterferon alfa-2b