Celiac disease and hepatitis C relationships in transcriptional regulatory networks

Fereshteh Izadi1, Mostafa Rezaei Tavirani2, Zahra Honarkar3,4

  • 1Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Insights

Network analysis revealed 105 common genes, including 11 transcription factors, linking celiac disease and hepatitis C. These genes highlight immune system pathways involved in inflammation, offering insights into disease comorbidities.

Area of Science:

  • Genomics and Bioinformatics
  • Immunology
  • Network Medicine

Background:

  • Celiac disease (CD) and hepatitis C (HCV) share unclear associations, impacting diagnosis and treatment.
  • HCV proteins may mimic gliadin, potentially triggering gluten intolerance in susceptible individuals.
  • Understanding the interplay between CD and HCV is crucial for discovering shared genetic regulators.

Purpose of the Study:

  • To elucidate potential comorbidities between celiac disease and hepatitis C.
  • To identify common genes and pathways linking these two conditions using network analysis.
  • To explore the functional roles of identified genes in disease pathogenesis.

Main Methods:

  • Retrieved 321 (CD) and 1032 (HCV) genes from DisGeNET.
  • Constructed a gene regulatory network using these genes.
  • Performed network-driven integrative analysis to identify prognostic genes and pathways.

Main Results:

  • Identified 105 common genes between CD and HCV, including 11 key transcription factors.
  • These genes are enriched in immune system pathways, including chemokines, cytokines, and interleukins.
  • The identified gene network highlights significant biological functions related to inflammation in both diseases.

Conclusions:

  • In silico analysis identified a core set of genes linking celiac disease and hepatitis C.
  • These genes are implicated in inflammatory processes relevant to both conditions.
  • The findings provide a foundation for further research into the molecular mechanisms underlying CD-HCV comorbidities.
Abstract

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