Abstract |
Epstein-Barr virus (EBV) uses nasal mucosa-associated lymphoid tissue (NALT) as a 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 beta(1) integrin, which is expressed the most by naïve B cells of distinct lymphoid origin and by memory B cells from NALT, as a mediator of increased susceptibility to infection by EBV. Furthermore, we show that BMRF-2-beta(1) integrin interaction and the downstream signal transduction pathway are critical for postbinding events. An increase of beta(1) 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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Authors | Marcus Dorner, Franziska Zucol, Davide Alessi, Stephan K Haerle, Walter Bossart, Markus Weber, Rahel Byland, Michele Bernasconi, Christoph Berger, Sharof Tugizov, Roberto F Speck, David Nadal |
Journal | Journal of virology
(J Virol)
Vol. 84
Issue 13
Pg. 6667-77
(Jul 2010)
ISSN: 1098-5514 [Electronic] United States |
PMID | 20427540
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- BMRF-2 protein, Human herpesvirus 4
- Integrin beta1
- Membrane Glycoproteins
- Viral Proteins
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Topics |
- B-Lymphocytes
(virology)
- Cell Line
- Herpesvirus 4, Human
(growth & development)
- Humans
- Integrin beta1
(biosynthesis)
- Membrane Glycoproteins
(metabolism)
- Protein Binding
- Protein Interaction Mapping
- Signal Transduction
- Viral Proteins
(metabolism)
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