PTPN22 C1858T polymorphism and the outcome of hepatitis C virus infection

Viral Immunol. 2008 Dec;21(4):491-4. doi: 10.1089/vim.2008.0040.


The outcome of chronic hepatitis C virus infection varies, depending on viral and host factors. Those mechanisms involved in the control of the innate and adaptive response could have an influence on the outcome of infection. The PTPN22 gene encodes an intracellular lymphoid-specific phosphatase (Lyp) with a lymphocyte activating downregulatory effect. A single-nucleotide polymorphism (SNP) C1858T located on this gene has been associated with autoimmune diseases and bacterial infections. The aim of this study was to assess whether the PTPN22 C1858T polymorphism is related to the outcome of hepatitis C viral infection. A total of 69 patients with spontaneous viral clearance (SVC), 281 patients with chronic hepatitis C (CHC), and 1036 individuals not infected with hepatitis C (NIC) were included in this study. Patients with CHC were stratified according to Scheuer score of hepatic fibrosis from F0-F2 (n = 200) and F3-F4 (n = 81), and according to their response to therapy in patients with sustained responses (SR; n = 103) and non-sustained response (NSR; n = 104). Genotyping of the C1858T polymorphism was performed using TaqMan probes. No statistically significant differences in the distribution of PTPN22 C1858T polymorphism were observed upon comparison of patient group with the NIC group. Also, when the different patient groups were compared to one another, no statistically significant differences were detected: the SVC with the CHC group (10.2% versus 12.5%; p = 0.6), the F0-F2 with the F3-F4 group (11.5% versus 14.8%; p = 0.5), and the NSR with the SR group (11.5% versus 14.6%; p = 0.4). Our results do not support a major role of this polymorphism of the PTPN22 gene in the outcome of chronic hepatitis C virus infection in the Spanish population.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Female
  • Genotype
  • Hepacivirus / pathogenicity*
  • Hepacivirus / physiology
  • Hepatitis C / genetics*
  • Hepatitis C / metabolism
  • Hepatitis C / virology
  • Host-Pathogen Interactions*
  • Humans
  • Male
  • Middle Aged
  • Mutation, Missense*
  • Polymorphism, Genetic*
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22 / genetics*
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22 / metabolism
  • White People / genetics


  • PTPN22 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22