Journal
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
Volume 35, Issue 6, Pages 592-602Publisher
WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1111/j.1365-2990.2009.01031.x
Keywords
blood-brain barrier; feline immunodeficiency virus; lymphocyte
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Funding
- National Neuroscience Network Grant through the Programme for Research in Third Level Institutions (Ireland)
- Science Foundation Ireland [06/RFP/BIM089]
- BBSRC [BB/D008425/1] Funding Source: UKRI
- MRC [G0300387] Funding Source: UKRI
- Science Foundation Ireland (SFI) [06/RFP/BIM089] Funding Source: Science Foundation Ireland (SFI)
- Biotechnology and Biological Sciences Research Council [BB/D008425/1] Funding Source: researchfish
- Medical Research Council [G0300387] Funding Source: researchfish
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Aims: In human immunodeficiency virus infection, macrophage-tropic and lymphotropic viruses exist in the host. Central nervous system (CNS) infection is an early and ongoing event, important to understand when developing strategies to treat infection. Some knowledge exists on macrophage-tropic virus interactions with the blood-brain barrier (BBB), and the aim of this study was to investigate lymphotropic lentivirus interactions with the BBB. Methods: Interactions of the lymphotropic feline immunodeficiency virus (FIV) with an in vitro model of the feline BBB were evaluated in scenarios to mimic in vivo infections. Results: Cell-free FIV crossed the BBB in very low quantities, and in the presence of tumour necrosis factor (TNF)-alpha, BBB integrity was unaffected. However, cell-associated FIV readily crossed the BBB, but BBB integrity was not significantly altered. Transmigration of uninfected and infected lymphocytes increased in response to TNF-alpha, accompanied by a moderate disruption of barrier integrity and an upregulation of vascular cell adhesion molecule-1 rather than intercellular adhesion molecule-1. Significant enhancement of migration and disruption of BBB tight junctions occurred when infected cells and TNF-alpha were added to the brain side of the BBB and this enhancement was not mediated through additional TNF-alpha production. Conclusions: Small quantities of virus in the brain together with TNF-alpha have the potential to stimulate greater cell and viral entry into the CNS and this is likely to involve important factors other than further TNF-alpha production. Lymphotropic lentivirus entry to the CNS is governed by many factors similar to macrophage-tropic strains.
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