Killer cell immunoglobulin-like receptors and response to antiviral treatment in Thai patients with chronic hepatitis C virus genotype 3a

J Med Virol. 2011 Oct;83(10):1733-7. doi: 10.1002/jmv.22153. Epub 2011 Jul 13.

Abstract

Genetic factors of the host have been shown to influence the outcome of treatment for hepatitis C virus (HCV) infection. Killer cell immunoglobulin-like receptors (KIR) regulate natural killer (NK) cell activity by interaction with specific human leukocyte antigen (HLA) class I. In this study, KIR gene polymorphisms and their HLA ligands were investigated in 110 Thai patients with chronic HCV genotype 3a. Seventy-six patients were sustained virological responders and 34 patients were virological non-responders. KIR typing and HLA-C typing were performed using PCR-SSP (polymerase chain reaction with sequence specific primer). The frequency of HLA-C1C2 was significantly higher in sustained responders than in non-responders (P = 0.04). However, the frequencies of KIR2DL2/2DL3 genotype and KIR2DL2/2DL3-HLA-C1C1 genotype were significantly higher in non-responders than in sustained responders (P = 0.02, 0.004, respectively). In summary, this study showed the association of KIR genes and ligands with the outcome of antiviral treatment in chronic hepatic C virus genotype 3a infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antiviral Agents / immunology
  • Antiviral Agents / therapeutic use*
  • Female
  • Genotype
  • HLA-A Antigens / genetics
  • HLA-C Antigens / genetics*
  • HLA-C Antigens / immunology
  • Hepacivirus / genetics
  • Hepacivirus / immunology
  • Hepatitis C, Chronic / drug therapy*
  • Hepatitis C, Chronic / immunology*
  • Humans
  • Killer Cells, Natural / immunology
  • Ligands
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide
  • Receptors, KIR / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Thailand
  • Treatment Outcome

Substances

  • Antiviral Agents
  • HLA-A Antigens
  • HLA-C Antigens
  • Ligands
  • Receptors, KIR