Downregulation of the stress-induced ligand ULBP1 following SV40 infection confers viral evasion from NK cell cytotoxicity

Oncotarget. 2016 Mar 29;7(13):15369-81. doi: 10.18632/oncotarget.8085.

Abstract

Polyomaviruses are a diverse family of viruses which are prevalent in the human population. However, the interactions of these viruses with the immune system are not well characterized. We have previously shown that two human polyomaviruses, JC and BK, use an identical microRNA to evade immune attack by Natural Killer (NK) cells. We showed that this viral microRNA suppresses ULBP3 expression, a stress induced ligand for the killer receptor NKG2D. Here we show that Simian Virus 40 (SV40) also evades NK cell attack through the down regulation of another stress-induced ligand of NKG2D, ULBP1. These findings indicate that NK cells play an essential role in fighting polyomavirus infections and further emphasize the importance of various members of the ULBP family in controlling polyomavirus infection.

Keywords: Immune response; Immunity; Immunology and Microbiology Section; NK cells; NKG2D; SV40; ULBP1; immune-evasion.

MeSH terms

  • Animals
  • Cell Line
  • Cytotoxicity, Immunologic / immunology*
  • Down-Regulation
  • GPI-Linked Proteins / biosynthesis
  • Humans
  • Immune Evasion / immunology*
  • Intracellular Signaling Peptides and Proteins / biosynthesis*
  • Killer Cells, Natural / immunology*
  • Polyomavirus Infections / immunology*
  • Simian virus 40 / immunology
  • Tumor Virus Infections / immunology*

Substances

  • GPI-Linked Proteins
  • Intracellular Signaling Peptides and Proteins
  • ULBP1 protein, human