I: ten.3389/fmicb.2014.Dendritic cells in the course of Epstein Barr virus infectionChristian M z*Viral Immunobiology, Institute of Experimental Immunology, University of Zurich, Zurich, SwitzerlandEdited by: Laura Hertel, Children’s Hospital Oakland Analysis Institute, USA Reviewed by: Stephen Gottschalk, Baylor College of Medicine, USA Andrew Hislop, University of Birmingham, UK *Correspondence: Christian M z, Viral Immunobiology, Institute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland e-mail: [email protected] Barr virus (EBV) causes persistent infection in additional than 90 on the human adult population and is associated with two of all tumors in humans. This -herpes virus infects primarily human B and epithelial cells, nevertheless it has been reported to be sensed by dendritic cells (DCs) during principal infection. These activated DCs are thought to contribute to innate restriction of EBV infection and initiate EBV-specific adaptive immune responses through crosspriming. The respective evidence and their possible importance for EBV-specific vaccine development will be discussed in this assessment.Search phrases: plasmacytoid dendritic cells, conventional dendritic cells, monocyte-derived dendritic cells, all-natural killer cells, T cellsINFECTION AND TUMORIGENESIS BY EPSTEIN BARR VIRUS Epstein Barr virus (EBV) was discovered 50 years ago in a cell line (EB1) from an African kid with Burkitt’s lymphoma (Epstein et al.951173-34-5 Purity , 1964). In spite of this association with lymphomas and carcinomas, which includes Hodgkin’s lymphoma and nasopharyngeal carcinoma (Kutok and Wang, 2006; Cesarman, 2014), EBV is carried with no symptoms by the vast majority of persistently infected individuals, which account for extra than 90 in the adult human population (Rickinson et al., 2014). EBV-associated malignancies arise with enhanced frequency in immunosuppressed patients, for example right after transplantation (post-transplant lymhoproliferative disease or PTLD), immunosuppressive co-infections for instance HIV, or main genetic immunodeficiencies (like X-linked lymphoproliferative disease or XLP).Price of 1446022-58-7 These findings indicate that asymptomatic chronic infection with EBV final results in component from continuous virus-specific immune manage.PMID:23075432 Mainly cellular immunity by all-natural killer (NK) and T cells appears to mediate this immune control (Rickinson et al., 2014), and a few EBV-associated malignancies can even be cured by adoptive transfer of EBVspecific T-cell lines (Gottschalk et al., 2005). Some proof has been provided that dendritic cells (DCs) sense EBV infection and are involved within the priming of those protective innate and adaptive immune responses. This proof and its relevance for EBV-specific vaccine improvement will likely be discussed in this evaluation. SELECTIVE HOST CELL TROPISM OF EBV Dendritic cells are possibly not initiating EBV-specific immune handle soon after obtaining straight infected by the virus. Although it has been reported that EBV can enter monocyte precursors of DCs, no EBV antigen expression may be discovered in these research and only CMV-promoter-driven green fluorescent protein (GFP) expression of recombinant EBV was detected after infection (Li et al., 2002; Guerreiro-Cacais et al., 2004). Certainly, the principle host cell of EBV could be the human B cell. In healthy EBV carriers, memory B cells seem to constitute the internet site of long-termpersistence (Babcock et al., 1998). Latency 0 in these memory B cells is associated with no viral protein expression but tra.