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Cell Rep. 2013 Dec 26;5(6):1489-98. doi: 10.1016/j.celrep.2013.11.041. Epub 2013 Dec 19.

Human natural killer cells prevent infectious mononucleosis features by targeting lytic Epstein-Barr virus infection.

Author information

1
Department of Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, 8057 Zürich, Switzerland.
2
DKFZ unit F100/INSERM unit U1074, 69120 Heidelberg, Germany.
3
Institute for Pathology, Unfallkrankenhaus Berlin, 12683 Berlin, Germany.
4
Laboratory of Applied Immunobiology, University of Zürich, 8006 Zürich, Switzerland.
5
Bone Marrow Transplantation Center, Instituto Nacional de Cancer (INCA), 20231-130 Rio de Janeiro, Brazil.
6
Dipartimento di Medicina Sperimentale, Università degli Studi di Genova, 16147 Genova, Italy; Centro di Eccellenza per le Ricerche Biomediche, Università degli Studi di Genova, 16147 Genova, Italy.
7
Institute of Medical Virology, University of Zürich, 8006 Zürich, Switzerland.
8
Department of Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, 8057 Zürich, Switzerland. Electronic address: christian.muenz@uzh.ch.

Erratum in

  • Cell Rep. 2015 Aug 4;12(5):901.

Abstract

Primary infection with the human oncogenic Epstein-Barr virus (EBV) can result in infectious mononucleosis (IM), a self-limiting disease caused by massive lymphocyte expansion that predisposes for the development of distinct EBV-associated lymphomas. Why some individuals experience this symptomatic primary EBV infection, whereas the majority acquires the virus asymptomatically, remains unclear. Using a mouse model with reconstituted human immune system components, we show that depletion of human natural killer (NK) cells enhances IM symptoms and promotes EBV-associated tumorigenesis mainly because of a loss of immune control over lytic EBV infection. These data suggest that failure of innate immune control by human NK cells augments symptomatic lytic EBV infection, which drives lymphocyte expansion and predisposes for EBV-associated malignancies.

PMID:
24360958
PMCID:
PMC3895765
DOI:
10.1016/j.celrep.2013.11.041
[Indexed for MEDLINE]
Free PMC Article
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