MxA expression as marker for assessing the therapeutic response in HCV genotype 4 Egyptian patients.
The prevalence of hepatitis C virus (HCV) infection varies across the world, with the highest number of infections reported in Egypt. Expression of the MxA gene has been found to be a reliable and sensitive marker for the induction of endogenous type I interferons (IFNs) during viral infections. This study examined the correlation of gene expression of MxA with the response to treatment with pegylated-IFN-alfa2b and ribavirin. Fifty patients with type 4 HCV and 20 healthy volunteers as controls were enrolled in a prospective study designed with strict inclusion criteria to nullify the effect of confounding variables and further minimize selection bias. Quantification of HCV-RNA and MxA gene by real-time PCR was performed for every patient, and quantification of MxA gene was performed for controls. There was a statistically significant difference between patients and control group as regards the quantity of MxA gene expression (P < 0.05) (Mann-Whitney test) (P = 0.004). There was a statistically significant difference between responders and nonresponders (P < 0.05): responders showed a higher percentage of cases with initial MxA <2(6) (P < 0.05). We conclude that MxA protein expression is a sensitive biological marker for ongoing virus replication and presence of type 1 IFN. These results highlight the importance of the detection of MxA expression at the start of therapy as a factor for assessing the likelihood of HCV genotype 4 patients to achieving a sustained virological response to treatment with IFN-α2 in combination with ribavirin.
Shaker
O
O
epartment of Medical Biochemistry, Faculty of Medicine, Cairo University, Cairo, Egypt.
Ahmed
A
A
Doss
W
W
Abdel-Hamid
M
M
D000293:Adolescent; D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D015415:Biomarkers; D016903:Drug Monitoring / Q000379:methods; D004534:Egypt; D005260:Female; D019204:GTP-Binding Proteins / Q000096:biosynthesis*; D015870:Gene Expression; D020869:Gene Expression Profiling; D005838:Genotype; D016174:Hepacivirus / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification; D006526:Hepatitis C / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D064547:Myxovirus Resistance Proteins; D011092:Polyethylene Glycols / Q000008:administration & dosage*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D012367:RNA, Viral / Q000097:blood / Q000235:genetics; D011994:Recombinant Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction; D019562:Viral Load; D055815:Young Adult
D000998:Antiviral Agents; D015415:Biomarkers; D000077190:Interferon alpha-2; D016898:Interferon-alpha; C579071:MX1 protein, human; D064547:Myxovirus Resistance Proteins; D012333:RNA, Messenger; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D019204:GTP-Binding Proteins; C417083:peginterferon alfa-2b