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Journal of Virology, July 2000, p. 6021-6030, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interactions between Brain Endothelial Cells and Human T-Cell Leukemia Virus Type 1-Infected Lymphocytes: Mechanisms of Viral Entry into the Central Nervous System

Ignacio A. Romero,1,* Marie-Christine Prevost,2 Emmanuelle Perret,2 Peter Adamson,3 John Greenwood,3 Pierre-Olivier Couraud,1,4 and Simona Ozden2

CNRS UPR 0415, Institut Cochin de Génétique Moléculaire, 75014 Paris,1 Unité d'Oncologie Virale, CNRS URA 1930, Institut Pasteur, 75724 Paris Cedex 15,2 and Neurotech S. A., Génopole Industries, 91000 Evry,4 France, and Department of Clinical Ophthalmology, Institute of Ophthalmology, London EC1V 9EL, United Kingdom3

Received 20 September 1999/Accepted 14 March 2000

Human T-cell leukemia virus type 1 (HTLV-1) is associated with a variety of clinical manifestations, including tropical spastic paraparesis or HTLV-1-associated myelopathy (TSP/HAM). Viral detection in the central nervous system (CNS) of TSP/HAM patients demonstrates the ability of HTLV-1 to cross the blood-brain barrier (BBB). To investigate viral entry into the CNS, rat brain capillary endothelial cells were exposed to human lymphocytes chronically infected by HTLV-1 (MT2), to lymphocytes isolated from a seropositive patient, or to a control lymphoblastoid cell line (CEM). An enhanced adhesion to and migration through brain endothelial cells in vitro was observed with HTLV-1-infected lymphocytes. HTLV-1-infected lymphocytes also induced a twofold increase in the paracellular permeability of the endothelial monolayer. These effects were associated with an increased production of tumor necrosis factor alpha by HTLV-1-infected lymphocytes in the presence of brain endothelial cells. Ultrastructural analysis showed that contact between endothelial cells and HTLV-1-infected lymphocytes resulted in a massive and rapid budding of virions from lymphocytes, followed by their internalization into vesicles by brain endothelial cells and apparent release onto the basolateral side, suggesting that viral particles may cross the BBB using the transcytotic pathway. Our study also demonstrates that cell-cell fusion occurs between HTLV-1-infected lymphocytes and brain endothelial cells, with the latter being susceptible to transient HTLV-1 infection. These aspects may help us to understand the pathogenic mechanisms associated with neurological diseases induced by HTLV-1 infection.

* Corresponding author. Present address: Department of Biological Sciences, Walton Hall, The Open University, Milton Keynes MK7 6AA, United Kingdom. Phone: 44-1908-659467. Fax: 44-1908-654167. E-mail: i.romero{at}open.ac.uk.

Journal of Virology, July 2000, p. 6021-6030, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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