title: [Genetic polymorphisms of MxA protein and eIF-2a-reg2 and their responses to interferon treatment in patients with chronic hepatitis B].
abstract: OBJECTIVE
  To identify the host single nucleotide polymorphisms (SNP) of myxovirus resistance A (MxA) protein and eukaryote initiation factor 2alfa regulatory region 2(eIF-2a-reg2) and to predict interferon (IFN) treatment responses in patients with chronic hepatitis B.
  
  
  METHODS
  Two hundred sixty-two patients with chronic hepatitis B (CHB) were treated with interferon alfa (IFN ) for 12 months. Six months later the therapeutic effectiveness was evaluated. All the patients had signed a formal consent form. The patients were grouped into a sustained response (SR) group and a non-sustained response (NSR) group according to their responses to the IFNa treatment. Single nucleotide polymorphisms of the antiviral protein MxA promoter -88,-123 and protein kinase(PKR) activated eIF-2a-reg2 sites were examined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and were compared with the responsiveness to IFN treatment of these CHB patients.
  
  
  RESULTS
  Among the 262 patients, 212 (80.9%) were non-sustained responders to IFNa and 50 (19.1%) were sustained responders. The rate of sustained responders with GT heterozygote at MxA promoter -88 was higher than that of the GG genotype (OR: 5.3, 95% CI: 2.46-11.43, P less than 0.01) and also higher than that of the TT genotype (OR: 4.1, 95% CI: 1.86-9.09, P less than 0.01). There were no statistically significant differences in IFN therapeutic effectiveness among the patients with different genotypes at MxA promoter -123, eIF-2a-reg2 and haplotypes made by MxA promoter -88 G/T, and -123 C/A alleles (P more than 0.05).
  
  
  CONCLUSIONS
  Patients with GT genotype at MxA promoter -88 responded well to IFN treatment. SNP as a potential marker could be used to predict IFN treatment responses of patients with chronic hepatitis B.
authors.affiliation: Beijing You'an Hospital, Capital University of Medical Sciences, Beijing 100069, China.
authors.forename: Yan-xiang
authors.initials: YX
authors.lastname: Huang
authors.forename: Li-na
authors.initials: LN
authors.lastname: Ma
authors.forename: Xin-yue
authors.initials: XY
authors.lastname: Chen
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Li
authors.forename: Yun-li
authors.initials: YL
authors.lastname: Huang
authors.forename: Cheng-li
authors.initials: CL
authors.lastname: Shen
authors.forename: Bing
authors.initials: B
authors.lastname: Ma
mesh_terms: D000293:Adolescent; D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D015852:Eukaryotic Initiation Factor-2 / Q000235:genetics*; D005260:Female; D019204:GTP-Binding Proteins / Q000235:genetics*; D005838:Genotype; D006515:Hepatitis B virus; D019694:Hepatitis B, Chronic / Q000188:drug therapy* / Q000235:genetics*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D064547:Myxovirus Resistance Proteins; D020641:Polymorphism, Single Nucleotide; D012045:Regulatory Sequences, Nucleic Acid / Q000235:genetics; D055815:Young Adult
chemical_list: D000998:Antiviral Agents; D015852:Eukaryotic Initiation Factor-2; D016898:Interferon-alpha; C579071:MX1 protein, human; D064547:Myxovirus Resistance Proteins; D019204:GTP-Binding Proteins