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Background <p>Hepatitis C virus (HCV) is a widespread global infection responsible for chronic liver disease, which can progress to fibrosis, cirrhosis, and hepatocellular carcinoma, influenced by viral, immune, and host genetic factors. Heme oxygenase-1 (HO-1) and adenosine deaminase acting on RNA 1 (ADAR1) are key regulators of antiviral immunity. Polymorphic variants in the <i>HO-1</i> and <i>ADAR1</i> genes (rs2071746 and rs1127313, respectively) may alter host susceptibility, viral replication, and the severity of hepatic injury, highlighting their potential as molecular markers of HCV pathogenesis in the Egyptian population.</p> Methods <p>Single-nucleotide polymorphisms (SNPs) were genotyped using TaqMan allelic discrimination assays in 100 participants, comprising 50 patients with chronic HCV infection and 50 healthy controls with comparable age and gender distribution. Clinical, biochemical, and virological assessments were conducted to evaluate hepatic status and viral load.</p> Results <p>The T allele of <i>HO-1</i> demonstrated a significant association with HCV susceptibility (OR = 4.89, <i>p</i> &lt; 0.001), with predominance of the AT genotype. The frequency of the G allele of <i>ADAR1</i> was significantly higher among patients (OR = 3.18, <i>p</i> &lt; 0.001). <i>HO-1</i> variants correlated with hepatic steatosis, higher FIB-4 scores, and increased liver enzyme levels, while polymorphisms of <i>ADAR1</i> showed no significant association with liver injury indices.</p> Conclusion <p>Polymorphisms in <i>HO-1</i> (rs2071746) and <i>ADAR1</i> (rs1127313) influence host susceptibility and disease progression in HCV infection. The <i>HO-1</i> T allele and AT genotype were strongly associated with HCV infection, whereas the <i>A</i> allele correlated with greater fibrosis and steatosis severity. Similarly, the <i>ADAR1</i> G allele and AG genotype were more prevalent in HCV patients and associated with higher viral loads, implicating ADAR1 in viral persistence and immune modulation. Those variants could potentially serve as genetic predictors for disease outcomes in HCV-infected individuals, warranting further large-scale studies.</p>

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HO-1 and ADAR1 gene polymorphisms in HCV-infected Egyptian cohort and its relation to disease severity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月24日

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  • Raghda Saad Zaghloul Taleb,
  • Walid Ibrahim Elsayed Yousif,
  • Marwa Deif,
  • Eman M. Osman,
  • Marwa Ibrahim Khedr,
  • Yara Safwat Roshdy,
  • Eman Saad Nassar

摘要

Background

Hepatitis C virus (HCV) is a widespread global infection responsible for chronic liver disease, which can progress to fibrosis, cirrhosis, and hepatocellular carcinoma, influenced by viral, immune, and host genetic factors. Heme oxygenase-1 (HO-1) and adenosine deaminase acting on RNA 1 (ADAR1) are key regulators of antiviral immunity. Polymorphic variants in the HO-1 and ADAR1 genes (rs2071746 and rs1127313, respectively) may alter host susceptibility, viral replication, and the severity of hepatic injury, highlighting their potential as molecular markers of HCV pathogenesis in the Egyptian population.

Methods

Single-nucleotide polymorphisms (SNPs) were genotyped using TaqMan allelic discrimination assays in 100 participants, comprising 50 patients with chronic HCV infection and 50 healthy controls with comparable age and gender distribution. Clinical, biochemical, and virological assessments were conducted to evaluate hepatic status and viral load.

Results

The T allele of HO-1 demonstrated a significant association with HCV susceptibility (OR = 4.89, p < 0.001), with predominance of the AT genotype. The frequency of the G allele of ADAR1 was significantly higher among patients (OR = 3.18, p < 0.001). HO-1 variants correlated with hepatic steatosis, higher FIB-4 scores, and increased liver enzyme levels, while polymorphisms of ADAR1 showed no significant association with liver injury indices.

Conclusion

Polymorphisms in HO-1 (rs2071746) and ADAR1 (rs1127313) influence host susceptibility and disease progression in HCV infection. The HO-1 T allele and AT genotype were strongly associated with HCV infection, whereas the A allele correlated with greater fibrosis and steatosis severity. Similarly, the ADAR1 G allele and AG genotype were more prevalent in HCV patients and associated with higher viral loads, implicating ADAR1 in viral persistence and immune modulation. Those variants could potentially serve as genetic predictors for disease outcomes in HCV-infected individuals, warranting further large-scale studies.