Authors:
Obinna Chijioke, Anne Müller, Regina Feederle, Mario Henrique M. Barros, Carsten Krieg, Vanessa Emmel, Emanuela Marcenaro, Carol S. Leung, Olga Antsiferova, Vanessa Landtwing, Walter Bossart, Alessandro Moretta, Rocio Hassan, Onur Boyman, Gerald Niedobitek, Henri-Jacques Delecluse, Riccarda Capaul, & Christian Münz
Summary:
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.
Source:
Cell Reports; Vol. 5, Issue 6, 1489-1498 (12/19/13)