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Journal of Virology, November 2008, p. 11273-11282, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.00775-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Measles Virus-Induced Block of Transendothelial Migration of T Lymphocytes and Infection-Mediated Virus Spread across Endothelial Cell Barriers{triangledown}

Sandra Dittmar,1 Harry Harms,1 Nicole Runkler,2 Andrea Maisner,2 Kwang Sik Kim,3 and Jürgen Schneider-Schaulies1*

Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany,1 Institute of Virology, University of Marburg, 35043 Marburg, Germany,2 Johns Hopkins University School of Medicine, Baltimore, Maryland 212873

Received 10 April 2008/ Accepted 27 August 2008

In order to analyze whether measles virus (MV) is transported via transmigrating leukocytes across endothelial barriers or whether virus spreads via infection of endothelial cells and basolateral release, we investigated the migratory behavior of infected human primary T lymphocytes across polarized cell layers of human brain microvascular endothelial cells. We found that the capacity of lymphocytes to migrate through filter pores was only slightly affected by wild-type MV infection, whereas their capacity to migrate through endothelial barriers was drastically reduced. MV infection stimulated the expression and activation of the leukocyte integrins LFA-1 and VLA-4, mediating a strong adherence to the surface of endothelial cells. Furthermore, the formation of engulfing membrane protrusions by endothelial cells, so-called transmigratory cups, was induced, but transmigration was impaired. As a consequence of this close cell-cell contact, MV infection was transmitted from lymphocytes to the endothelium. MV envelope proteins were expressed on the apical and basolateral surfaces of infected polarized endothelial cells, and virus was released from both sides. Wild-type MV infection did not induce the formation of syncytia, suggesting virus spread from cell to cell via cell processes and contacts. Our data indicate that transendothelial migration of infected T cells is strongly inhibited, whereas virus can cross endothelial barriers by productive infection of the endothelium and subsequent bipolar virus release.

* Corresponding author. Mailing address: Institut für Virologie und Immunbiologie, Versbacher Str. 7, 97078 Würzburg, Germany. Phone: 49-931-20149895. Fax: 49-931-20149553. E-mail: jss{at}vim.uni-wuerzburg.de

{triangledown} Published ahead of print on 3 September 2008.

Journal of Virology, November 2008, p. 11273-11282, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.00775-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Abt, M., Gassert, E., Schneider-Schaulies, S. (2009). Measles virus modulates chemokine release and chemotactic responses of dendritic cells. J. Gen. Virol. 90: 909-914 [Abstract] [Full Text]  


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