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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.

Original publication

DOI

10.1016/j.celrep.2013.11.041

Type

Journal article

Journal

Cell reports

Publication Date

12/2013

Volume

5

Pages

1489 - 1498

Addresses

Department of Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, 8057 Zürich, Switzerland.

Keywords

Killer Cells, Natural, Animals, Mice, Inbred NOD, Humans, Mice, Mice, SCID, Infectious Mononucleosis, Trans-Activators, Immunologic Memory, Immunity, Innate, Carcinogenesis