beta1 integrin expression increases susceptibility of memory B cells to Epstein-Barr virus infection.

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.

• 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)

Chemical References

• BMRF-2 protein, Human herpesvirus 4
• Integrin beta1
• Membrane Glycoproteins
• Viral Proteins

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)