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

Yoav Bauman, Nir Drayman, Orly Ben-Nun-Shaul, Alon Vitenstein, Rachel Yamin, Yael Ophir, Ariella Oppenheim, Ofer Mandelboim*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

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.

Original languageAmerican English
Pages (from-to)15369-15381
Number of pages13
JournalOncotarget
Volume7
Issue number13
DOIs
StatePublished - 29 Mar 2016

Keywords

  • Immune response
  • Immune-evasion
  • Immunity
  • Immunology and microbiology section
  • NK cells
  • NKG2D
  • SV40
  • ULBP1

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