title: [Association between single nucleotide polymorphisms in -88 and -123 loci of MxA gene promoter region and HCV susceptibility and IFN-α efficacy].
abstract: OBJECTIVE
  To investigate the association between the single nucleotide polymorphisms(SNP) in -88 and -123 loci of myxovirus resistance 1(MxA) gene promoter region and the susceptibility to heptaitis C virus(HCV) in Han Chinese,  and evaluate the relationship between all of the genotypes and the treatment response to IFN-α.
  
  
  METHODS
  Genotypes of -88(G/T) and -123(C/A) loci of the MxA promoter were examined by the polymerase chain reaction and restriction fragment length polymorphism(PCR-RFLP) in 46 patients with chronic hepatitis C(CHC group) and 50 healthy controls(HC group). The indexes for evaluating the curative effect were the biochemical and virological response rates(RVR/EVR/ETVR/SVR).
  
  
  RESULTS
  There was no statistical significance in frequency distribution difference of the genotypes and alleles of -88/-123 loci between CHC and CH groups(P>0.05):  the T-alleles of MxA-88 locus and the A-alleles of MxA-123 locus may be not associated with the susceptibility to HCV(OR95%CI:  0.60-1.96,  0.35-1.14,  respectively). The level of ALT increased and was positively correlated with HCV-RNA load(r=0.931). No significant difference was discovered in terms of the HCV viral load and the ALT levels among different genotypes of -88 or -123 loci(P>0.05). IFN-α treatment response rates were also not significantly different among -88G/T,  -123C/A and MxA-88/-123(P>0.05).
  
  
  CONCLUSIONS
  There is no distinct correlation between the SNP of MxA-88G/T and MxA-123C/A loci and HCV susceptibility,  but the MxA-88T/-123A gene variants may indirectly increase the risk for HCV infection,  and the MxA-88T gene mutation may be related to IFN-α antiviral efficacy and the outcomes of HCV infection.
authors.affiliation: Department of Clinical Laboratory,  Hubei University of Medicine,  Affiliated Taihe Hospital,     Shiyan 442000,  China.
authors.forename: Chun-hui
authors.initials: CH
authors.lastname: Hu
authors.forename: Jin
authors.initials: J
authors.lastname: Chen
authors.forename: Rui
authors.initials: R
authors.lastname: Yang
authors.forename: Nan-nan
authors.initials: NN
authors.lastname: Li
authors.forename: Bo
authors.initials: B
authors.lastname: Yang
authors.forename: Dan
authors.initials: D
authors.lastname: Ma
authors.forename: Xiao-cui
authors.initials: XC
authors.lastname: Liang
authors.forename: Qun
authors.initials: Q
authors.lastname: Wang
mesh_terms: D000328:Adult; D000483:Alleles; D000998:Antiviral Agents / Q000627:therapeutic use; D044466:Asian People / Q000208:ethnology / Q000235:genetics; D002681:China / Q000208:ethnology; D005260:Female; D019204:GTP-Binding Proteins / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D005838:Genotype; D016174:Hepacivirus / Q000502:physiology*; D006526:Hepatitis C / Q000188:drug therapy* / Q000208:ethnology / Q000235:genetics*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D064547:Myxovirus Resistance Proteins; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; C579071:MX1 protein, human; D064547:Myxovirus Resistance Proteins; D019204:GTP-Binding Proteins