Research Papers: Immunology:

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 and Ofer Mandelboim

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Oncotarget. 2016; 7:15369-15381. https://doi.org/10.18632/oncotarget.8085

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Yoav Bauman1, Nir Drayman2, Orly Ben-Nun-Shaul2 Alon Vitenstein1, Rachel Yamin1, Yael Ophir1, Ariella Oppenheim2,* and Ofer Mandelboim1,*

1 The Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel-Canada of The Faculty of Medicine (IMRIC), The Hebrew University Hadassah Medical School, Jerusalem, Israel

2 Department of Hematology Hebrew University-Hadassah Medical School, Jerusalem, Israel

* The authors have contributed equally to this work

Correspondence to:

Ofer Mandelboim, email:

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

Received: December 03, 2015 Accepted: February 23, 2016 Published: March 15, 2016


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.

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