title: CCL2-2518 A/G and CCR2 190 A/G do not influence the outcome of hepatitis C virus infection in the Spanish population.
abstract: OBJECTIVE
  To assess whether CCL2 or interactions between this chemokine and its receptor (CCR2) are associated with outcomes of chronic hepatitis C and with responses to antiviral therapy.
  
  
  METHODS
  Two hundred and eighty-four patients with chronic hepatitis C and 193 non-infected matched controls were included in this study. Patients were categorized according to their Scheuer score of hepatic fibrosis as F0-F2 (n = 202) or F3-F4 (n = 82) and according to their response to anti-Hepatitis C virus (HCV) therapy as sustained response (SR, n = 101) or non-sustained response (NSR, n = 98). Genotyping of the -2518 (A/G) CCL2 was performed using PCR-RFLP, genotyping of the 190 (A/G) CCR2 using a PCR-ARMS system, and genotyping of the rs3138042 (G/A) CCR2 using Taqman probes.
  
  
  RESULTS
  Univariate analyses identified 4 parameters (infection duration time, viral genotype, gender and AST levels) that tended to influence fibrosis and 7 parameters (CCL2G, CCL2ACCR2A, viremia levels, fibrosis stage, viral genotype, infection duration time and AST levels) that significantly influenced or tended to influence response to treatment. Multivariate analysis identified gender and AST levels as parameters that independently influenced fibrosis stage and viral genotype and infection duration time were the two parameters that independently influenced response to treatment.
  
  
  CONCLUSIONS
  Our results indicate that the mutations studied in the gene pair CCL2/CCR2 do not play a major role in the outcome and response to treatment for HCV infection in the Spanish population.
authors.affiliation: Servicio de Inmunologia, Hospital Universitario Virgen del Rocio, Seville 41013, Spain.
authors.forename: M-A
authors.initials: MA
authors.lastname: Montes-Cano
authors.forename: J-R
authors.initials: JR
authors.lastname: Garcia-Lozano
authors.forename: J
authors.initials: J
authors.lastname: Aguilar-Reina
authors.forename: M
authors.initials: M
authors.lastname: Romero-Gomez
authors.forename: N
authors.initials: N
authors.lastname: Barroso
authors.forename: A
authors.initials: A
authors.lastname: Nunez-Roldan
authors.forename: M-F
authors.initials: MF
authors.lastname: Gonzalez-Escribano
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D001706:Biopsy; D018932:Chemokine CCL2 / Q000235:genetics / Q000502:physiology*; D005260:Female; D005838:Genotype; D006526:Hepatitis C / Q000188:drug therapy* / Q000208:ethnology / Q000235:genetics; D006801:Humans; D007370:Interferon Type I / Q000627:therapeutic use*; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009154:Mutation / Q000235:genetics; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000235:genetics / Q000502:physiology*; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use*; D013030:Spain; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; C111835:CCL2 protein, human; C515334:CCR2 protein, human; D018932:Chemokine CCL2; D007370:Interferon Type I; D054390:Receptors, CCR2; D019707:Receptors, Chemokine; D011994:Recombinant Proteins; D012254:Ribavirin