Background <p>Genetic polymorphisms within the tumor necrosis factor (TNF) cluster have been implicated in several diseases. This exploratory study aimed to assess the role of two polymorphisms (− 308G &gt; A and − 857&#xa0;C &gt; T) in the TNF-α gene in the risk of developing chronic Hepatitis B virus (CHB) infection in a cohort of Mauritanian patients.</p> Methods <p>We selected 160 subjects, including 82 patients with CHB and 78 spontaneously cured controls. Following PCR amplification, the targeted DNA regions were sequenced using the Sanger method.</p> Results <p>The TNF-α-308 G &gt; A (rs1800629) wild-type GG genotype was significantly associated with decreased susceptibility to CHB (OR = 0.13 (0.045–0.379), <i>p</i> &lt; 0.001). In contrast, the A mutant allele was identified as a risk factor for HBV persistence (OR = 0.310 (0.132–0.728), <i>p</i> = 0.007). The TNF-α-857&#xa0;C &gt; T (rs1799724) polymorphism was not associated with CHB, although the minor allele T was linked with a high viral load (OR = 0.14(0.03–0.76), <i>p</i> = 0.022).</p> Conclusion <p>Our results suggest a possible association between TNF-α-308 G &gt; A (rs1800629) variation and the evolution of HBV infection to a chronic state in Mauritanian patients.</p>

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Impact of TNF-α (− 308G>A and − 857 C>T) promoter variants on susceptibility to chronic hepatitis B virus infection in a cohort of Mauritanian patients: pilot study

  • Saffiya Mounira Ennahoui,
  • Abdallah Sid M’Hamed,
  • Fatimetou Veten,
  • Sidi M. Cheikh Bouna,
  • Abdelhamid Barakat,
  • Tetou Soumbara,
  • Ahmed Houmeida

摘要

Background

Genetic polymorphisms within the tumor necrosis factor (TNF) cluster have been implicated in several diseases. This exploratory study aimed to assess the role of two polymorphisms (− 308G > A and − 857 C > T) in the TNF-α gene in the risk of developing chronic Hepatitis B virus (CHB) infection in a cohort of Mauritanian patients.

Methods

We selected 160 subjects, including 82 patients with CHB and 78 spontaneously cured controls. Following PCR amplification, the targeted DNA regions were sequenced using the Sanger method.

Results

The TNF-α-308 G > A (rs1800629) wild-type GG genotype was significantly associated with decreased susceptibility to CHB (OR = 0.13 (0.045–0.379), p < 0.001). In contrast, the A mutant allele was identified as a risk factor for HBV persistence (OR = 0.310 (0.132–0.728), p = 0.007). The TNF-α-857 C > T (rs1799724) polymorphism was not associated with CHB, although the minor allele T was linked with a high viral load (OR = 0.14(0.03–0.76), p = 0.022).

Conclusion

Our results suggest a possible association between TNF-α-308 G > A (rs1800629) variation and the evolution of HBV infection to a chronic state in Mauritanian patients.