Tags

Type your tag names separated by a space and hit enter

Immune activation suppresses initiation of lytic Epstein-Barr virus infection.
Cell Microbiol 2007; 9(8):2055-69CM

Abstract

Primary infection with Epstein-Barr virus (EBV) is asymptomatic in children with immature immune systems but may manifest as infectious mononucleosis, a vigorous immune activation, in adolescents or adults with mature immune systems. Infectious mononucleosis and chronic immune activation are linked to increased risk for EBV-associated lymphoma. Here we show that EBV initiates progressive lytic infection by expression of BZLF-1 and the late lytic genes gp85 and gp350/220 in cord blood mononuclear cells (CBMC) but not in peripheral blood mononuclear cells (PBMC) from EBV-naive adults after EBV infection ex vivo. Lower levels of proinflammatory cytokines in CBMC, used to model a state of minimal immune activation and immature immunity, than in PBMC were associated with lytic EBV infection. Triggering the innate immunity specifically via Toll-like receptor-9 of B cells substantially suppressed BZLF-1 mRNA expression in acute EBV infection ex vivo and in anti-IgG-stimulated chronically latently EBV-infected Akata Burkitt lymphoma cells. This was mediated in part by IL-12 and IFN-gamma. These results identify immune activation as critical factor for the suppression of initiation of lytic EBV infection. We hypothesize that immune activation contributes to EBV-associated lymphomagenesis by suppressing lytic EBV and in turn promotes latent EBV with transformation potential.

Authors+Show Affiliations

Laboratory for Experimental Infectious Diseases and Cancer Research of the Division of Infectious Diseases, University Children's Hospital of Zurich, 8032 Zurich, Switzerland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17419714

Citation

Ladell, Kristin, et al. "Immune Activation Suppresses Initiation of Lytic Epstein-Barr Virus Infection." Cellular Microbiology, vol. 9, no. 8, 2007, pp. 2055-69.
Ladell K, Dorner M, Zauner L, et al. Immune activation suppresses initiation of lytic Epstein-Barr virus infection. Cell Microbiol. 2007;9(8):2055-69.
Ladell, K., Dorner, M., Zauner, L., Berger, C., Zucol, F., Bernasconi, M., ... Nadal, D. (2007). Immune activation suppresses initiation of lytic Epstein-Barr virus infection. Cellular Microbiology, 9(8), pp. 2055-69.
Ladell K, et al. Immune Activation Suppresses Initiation of Lytic Epstein-Barr Virus Infection. Cell Microbiol. 2007;9(8):2055-69. PubMed PMID: 17419714.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immune activation suppresses initiation of lytic Epstein-Barr virus infection. AU - Ladell,Kristin, AU - Dorner,Marcus, AU - Zauner,Ludwig, AU - Berger,Christoph, AU - Zucol,Franziska, AU - Bernasconi,Michele, AU - Niggli,Felix K, AU - Speck,Roberto F, AU - Nadal,David, Y1 - 2007/04/05/ PY - 2007/4/11/pubmed PY - 2008/2/13/medline PY - 2007/4/11/entrez SP - 2055 EP - 69 JF - Cellular microbiology JO - Cell. Microbiol. VL - 9 IS - 8 N2 - Primary infection with Epstein-Barr virus (EBV) is asymptomatic in children with immature immune systems but may manifest as infectious mononucleosis, a vigorous immune activation, in adolescents or adults with mature immune systems. Infectious mononucleosis and chronic immune activation are linked to increased risk for EBV-associated lymphoma. Here we show that EBV initiates progressive lytic infection by expression of BZLF-1 and the late lytic genes gp85 and gp350/220 in cord blood mononuclear cells (CBMC) but not in peripheral blood mononuclear cells (PBMC) from EBV-naive adults after EBV infection ex vivo. Lower levels of proinflammatory cytokines in CBMC, used to model a state of minimal immune activation and immature immunity, than in PBMC were associated with lytic EBV infection. Triggering the innate immunity specifically via Toll-like receptor-9 of B cells substantially suppressed BZLF-1 mRNA expression in acute EBV infection ex vivo and in anti-IgG-stimulated chronically latently EBV-infected Akata Burkitt lymphoma cells. This was mediated in part by IL-12 and IFN-gamma. These results identify immune activation as critical factor for the suppression of initiation of lytic EBV infection. We hypothesize that immune activation contributes to EBV-associated lymphomagenesis by suppressing lytic EBV and in turn promotes latent EBV with transformation potential. SN - 1462-5814 UR - https://www.unboundmedicine.com/medline/citation/17419714/Immune_activation_suppresses_initiation_of_lytic_Epstein_Barr_virus_infection_ L2 - https://doi.org/10.1111/j.1462-5822.2007.00937.x DB - PRIME DP - Unbound Medicine ER -