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{beta}1 Integrin Expression Increases Susceptibility of Memory B-Cells to EBV Infection


Dorner, M; Zucol, F; Alessi, D; Haerle, S K; Bossart, W; Weber, M; Byland, R; Bernasconi, M; Berger, C; Tugizov, S; Speck, R F; Nadal, D (2010). {beta}1 Integrin Expression Increases Susceptibility of Memory B-Cells to EBV Infection. Journal of Virology, 84(13):6667-6677.

Abstract

The Epstein-Barr virus (EBV) uses nasopharyngeal-associated lymphoid tissue (NALT) as portal of entry to establish life-long persistence in memory B-cells. We previously showed that naïve and memory B-cells from NALT are equally susceptible to EBV infection. Here, we show that memory B-cells from NALT are significantly more susceptible to EBV infection than those from remote lymphatic organs. We identify beta1 integrin, which is expressed highest by naïve B-cells of distinct lymphoid origin and by memory B-cells from NALT, as mediator of increased susceptibility to infection by EBV. Furthermore, we show that BMRF-2-beta1 integrin interaction and the downstream signal transduction pathway is critical for post-binding events. Increase of beta1 integrin expression in peripheral blood memory B-cells provoked by CD40 stimulation plus B-cell receptor cross-linking increased the susceptibility of non-NALT memory B-cells to EBV infection. Thus, EBV seems to utilize the increased activation status of memory B-cells residing in the NALT to establish and ensure persistence.

Abstract

The Epstein-Barr virus (EBV) uses nasopharyngeal-associated lymphoid tissue (NALT) as portal of entry to establish life-long persistence in memory B-cells. We previously showed that naïve and memory B-cells from NALT are equally susceptible to EBV infection. Here, we show that memory B-cells from NALT are significantly more susceptible to EBV infection than those from remote lymphatic organs. We identify beta1 integrin, which is expressed highest by naïve B-cells of distinct lymphoid origin and by memory B-cells from NALT, as mediator of increased susceptibility to infection by EBV. Furthermore, we show that BMRF-2-beta1 integrin interaction and the downstream signal transduction pathway is critical for post-binding events. Increase of beta1 integrin expression in peripheral blood memory B-cells provoked by CD40 stimulation plus B-cell receptor cross-linking increased the susceptibility of non-NALT memory B-cells to EBV infection. Thus, EBV seems to utilize the increased activation status of memory B-cells residing in the NALT to establish and ensure persistence.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Medical Virology
04 Faculty of Medicine > University Hospital Zurich > Clinic for Otorhinolaryngology
04 Faculty of Medicine > University Hospital Zurich > Clinic for Infectious Diseases
04 Faculty of Medicine > University Children's Hospital Zurich > Medical Clinic
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:July 2010
Deposited On:21 May 2010 11:55
Last Modified:03 Aug 2017 15:16
Publisher:American Society for Microbiology
ISSN:0022-538X
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1128/JVI.02675-09
PubMed ID:20427540

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