IL28B, TLR7 SNPs, and cytomegalovirus infection are risk factors for advanced liver disease in chronic hepatitis C patients

Expert Rev Anti Infect Ther. 2022 Jan;20(1):121-129. doi: 10.1080/14787210.2021.1935239. Epub 2021 Jun 7.

Abstract

Background: Chronic hepatitis C (CHC) is a leading cause of cirrhosis and hepatocellular carcinoma (HCC). This study aimed to study the association of IL28B, toll-like receptor (TLR) 7, cytomegalovirus and advanced liver disease.

Methods: Four groups were included; control (n = 125, 25.9%), CHC (n = 114, 23.6%), liver cirrhosis (n = 120, 24.8%), and HCC (n = 124, 25.7%).

Results: In CHC group, patients were mainly F1 (60%) followed by F2. IL28B genotype CC percentage was higher in control group than the CHC and cirrhosis groups. CT and TT genotypes were higher in the CHC and cirrhosis groups than control group. The C allele was higher in the control group than the CHC, cirrhosis and HCC groups and the opposite with the T allele. Control and CHC had same TLR7 alleles. Cirrhosis patients and HCC had lower TLR 7 A allele and higher G allele than the control group. Both cirrhosis and HCC groups had statistically significant higher percentage of the AG and GG genotypes than the control group. Patients with HCC had higher cytomegalovirus infection percentage than cirrhosis and CHC group (38.7% vs 20% vs 16.7%), respectively.

Conclusion: IL28B, TLR7 SNPs and cytomegalovirus infection are risk factors for advanced liver disease in hepatitis C patients.

Keywords: Hepatitis C virus; cytomegalovirus; hepatocellular carcinoma; interleukin 28B; toll-like receptor 7.

MeSH terms

  • Carcinoma, Hepatocellular* / etiology
  • Carcinoma, Hepatocellular* / genetics
  • Cytomegalovirus Infections* / complications
  • Cytomegalovirus Infections* / genetics
  • Genotype
  • Hepatitis C, Chronic* / complications
  • Hepatitis C, Chronic* / genetics
  • Humans
  • Interferons / genetics
  • Interleukins / genetics
  • Liver Cirrhosis / genetics
  • Liver Neoplasms* / etiology
  • Liver Neoplasms* / genetics
  • Polymorphism, Single Nucleotide
  • Risk Factors
  • Toll-Like Receptor 7 / genetics

Substances

  • interferon-lambda, human
  • Interleukins
  • TLR7 protein, human
  • Toll-Like Receptor 7
  • Interferons