Associations of content and gene polymorphism of macrophage inhibitory factor-1 and chronic hepatitis C virus infection
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Published on: October 1, 2015
Xun-Jun Yang1, Xiao-Ou Wang1, Yao Chen2
1Department of Laboratory Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, Zhejiang Province, China.
Insights
Macrophage inhibitory factor-1 (MIC-1) levels are elevated in chronic hepatitis C (CHC) patients and linked to disease severity. MIC-1 gene polymorphism at rs1059519 is associated with CHC susceptibility and MIC-1 levels.
Area of Science:
- Genetics
- Hepatology
- Immunology
Background:
- Macrophage inhibitory factor-1 (MIC-1) expression is elevated in chronic hepatitis and liver cirrhosis.
- The association between MIC-1 gene polymorphism and these diseases remains uninvestigated.
Purpose of the Study:
- To investigate the correlation between MIC-1 gene exon polymorphism and chronic hepatitis C virus (HCV) infection.
- To assess the relationship between MIC-1 levels, gene variants, and disease markers in CHC.
Main Methods:
- A case-control study involving 178 CHC patients and 82 healthy controls.
- DNA sequencing to determine genotypes at MIC-1 rs1059369 and rs1059519 loci.
- Measurement of plasma MIC-1, liver function tests, fibrosis markers, and HCV RNA load, followed by statistical analysis.
Main Results:
- CHC patients exhibited higher plasma MIC-1 levels, positively correlated with liver damage markers (ALT, AST), fibrosis indicators (PIIINP, Type IV collagen), and HCV RNA load.
- Significant differences in genotype and allele frequencies at the MIC-1 rs1059519 locus were observed between CHC patients and controls, with the G allele and GG genotype identified as independent risk factors.
- MIC-1 levels increased with rs1059519 genotypes, notably higher in the GG genotype.
Conclusions:
- Elevated plasma MIC-1 levels in CHC patients correlate with liver damage, fibrosis, and viral load.
- Polymorphism in the MIC-1 gene (rs1059519) is linked to HCV infection and influences plasma MIC-1 levels.
- The G allele and GG genotype of MIC-1 rs1059519 may represent a significant susceptibility factor for CHC.
Background:
The expression of macrophage inhibitory factor-1 (MIC-1) is increased in peripheral blood of patients with chronic hepatitis and liver cirrhosis. However, whether MIC-1 gene polymorphism is correlated with relevant diseases is not yet reported.
Aim:
To explore the correlation between gene polymorphism in MIC-1 exon region and chronic hepatitis C virus (HCV) infection.
Methods:
This case-control study enrolled 178 patients with chronic hepatitis C (CHC) in the case group, and 82 healthy subjects from the same region who had passed the screening examination comprised the control group. The genotypes of rs1059369 and rs1059519 loci in the MIC-1 gene exon were detected by DNA sequencing. Also, the MIC-1 level, liver function metrics, liver fibrosis metrics, and HCV RNA load were determined. Univariate analysis was used to compare the differences and correlations between the two groups with respect to these parameters. Multivariate logistic regression was used to analyze the independent relevant factors of CHC.
Results:
The plasma MIC-1 level in the CHC group was higher than that in the control group (P < 0.05), and it was significantly positively correlated with alanine aminotransferase, aspartate aminotransferase (AST), type III procollagen N-terminal peptide (known as PIIINP), type IV collagen, and HCV RNA (P < 0.05), whereas negatively correlated with total protein and albumin (P < 0.05). The genotype and allele frequency distribution at the rs1059519 locus differed between the two groups (P < 0.05). The allele frequency maintained significant difference after Bonferroni correction (Pc < 0.05). Logistic multiple regression showed that AST, PIIINP, MIC-1, and genotype GG at the rs1059519 locus were independent relevant factors of CHC (P < 0.05). Linkage disequilibrium (LD) was found between rs1059369 and rs1059519 loci, and significant difference was detected in the distribution of haplotype A-C between the CHC and control groups (P < 0.05). Meanwhile, we found the MIC-1 level trend to increase among rs1059519 genotypes (P = 0.006) and the level of MIC-1 in GG genotype to be significantly higher than CC genotype (P = 0.009, after Bonferroni correction).
Conclusion:
Plasma MIC-1 level was increased in CHC patients and correlated with liver cell damage, liver fibrosis metrics, and viral load. The polymorphism at the MIC-1 gene rs1059519 locus was correlated with HCV infection, and associated with the plasma MIC-1 level. G allele and GG genotype may be an important susceptible factor for CHC.
