Objectives: 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).
Conclusion: 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.