HCV RNA Activates APCs via TLR7/TLR8 While Virus Selectively Stimulates Macrophages Without Inducing Antiviral Responses

Sci Rep. 2016 Jul 7:6:29447. doi: 10.1038/srep29447.

Abstract

The innate and adaptive immune systems fail to control HCV infection in the majority of infected individuals. HCV is an ssRNA virus, which suggests a role for Toll-like receptors (TLRs) 7 and 8 in initiating the anti-viral response. Here we demonstrate that HCV genomic RNA harbours specific sequences that initiate an anti-HCV immune response through TLR7 and TLR8 in various antigen presenting cells. Conversely, HCV particles are detected by macrophages, but not by monocytes and DCs, through a TLR7/8 dependent mechanism; this leads to chloroquine sensitive production of pro-inflammatory cytokines including IL-1β, while the antiviral type I Interferon response is not triggered in these cells. Antibodies to DC-SIGN, a c-type lectin selectively expressed by macrophages but not pDCs or mDCs, block the production of cytokines. Novel anti-HCV vaccination strategies should target the induction of TLR7/8 stimulation in APCs in order to establish potent immune responses against HCV.

MeSH terms

  • Antigen-Presenting Cells / immunology
  • Antigen-Presenting Cells / virology*
  • Cell Line
  • Chloroquine / pharmacology
  • HEK293 Cells
  • Hepacivirus / genetics*
  • Hepacivirus / immunology
  • Hepatitis C / immunology
  • Humans
  • Interleukin-1beta / metabolism
  • Macrophages / metabolism
  • Macrophages / virology*
  • RNA, Viral / immunology*
  • Toll-Like Receptor 7 / metabolism*
  • Toll-Like Receptor 8 / metabolism*

Substances

  • IL1B protein, human
  • Interleukin-1beta
  • RNA, Viral
  • TLR7 protein, human
  • TLR8 protein, human
  • Toll-Like Receptor 7
  • Toll-Like Receptor 8
  • Chloroquine