title: Innate Immune Recognition of EBV.
abstract: The ability of Epstein-Barr virus (EBV) to establish latency despite specific immune responses and to successfully persist lifelong in the human host shows that EBV has developed powerful strategies and mechanisms to exploit, evade, abolish, or downsize otherwise effective immune responses to ensure its own survival. This chapter focuses on current knowledge on innate immune responses against EBV and its evasion strategies for own benefit and summarizes the questions that remain to be tackled. Innate immune reactions against EBV originate both from the main target cells of EBV and from nontarget cells, which are elements of the innate immune system. Thus, we structured our review accordingly but with a particular focus on the innate recognition of EBV in its two stages in its life cycle, latent state and lytic replication. Specifically, we discuss (I) innate sensing and resulting innate immune responses against EBV by its main target cells, focusing on (i) EBV transmission between epithelial cells and B cells and their life cycle stages; and (ii) elements of innate immunity in EBV's target cells. Further, we debate (II) the innate recognition and resulting innate immune responses against EBV by cells other than the main target cells, focusing on (iii) myeloid cells: dendritic cells, monocytes, macrophages, and neutrophil granulocytes; and (iv) natural killer cells. Finally, we address (III) how EBV counteracts or exploits innate immunity in its latent and lytic life cycle stages, concentrating on (v) TLRs; (vi) EBERs; and (vii) microRNAs.
authors.affiliation: Division of Infectious Diseases and Hospital Epidemiology, University Children's Hospital of Zurich, Steinwiesstrasse 75, 8032, Zurich, Switzerland.|Children's Research Center, University Children's Hospital of Zurich, Zurich, Switzerland.
authors.forename: Anna
authors.initials: A
authors.lastname: Lünemann
authors.affiliation: Centre for Human Virology, School of Cancer Sciences, College of Medical and Dental Sciences, The University of Birmingham, Birmingham, UK.
authors.forename: Martin
authors.initials: M
authors.lastname: Rowe
authors.affiliation: Division of Infectious Diseases and Hospital Epidemiology, University Children's Hospital of Zurich, Steinwiesstrasse 75, 8032, Zurich, Switzerland. david.nadal@kispi.uzh.ch.|Children's Research Center, University Children's Hospital of Zurich, Zurich, Switzerland. david.nadal@kispi.uzh.ch.
authors.forename: David
authors.initials: D
authors.lastname: Nadal
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology / Q000821:virology; D003713:Dendritic Cells / Q000276:immunology / Q000821:virology; D020031:Epstein-Barr Virus Infections / Q000276:immunology* / Q000821:virology; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology / Q000821:virology; D008264:Macrophages / Q000276:immunology / Q000821:virology
keywords: B cells; Epithelial cells; Natural killer cells; Toll-like receptors; microRNA