This article is a US Government work and, as such, is in the public domain in the United States of America.
CD46 on glial cells can function as a receptor for viral glycoprotein-mediated cell–cell fusion†
Article first published online: 26 MAY 2005
Published 2005 Wiley-Liss, Inc.
Volume 52, Issue 3, pages 252–258, 15 November 2005
How to Cite
Cassiani-Ingoni, R., Greenstone, H. L., Donati, D., Fogdell-Hahn, A., Martinelli, E., Refai, D., Martin, R., Berger, E. A. and Jacobson, S. (2005), CD46 on glial cells can function as a receptor for viral glycoprotein-mediated cell–cell fusion. Glia, 52: 252–258. doi: 10.1002/glia.20219
- Issue published online: 29 SEP 2005
- Article first published online: 26 MAY 2005
- Manuscript Accepted: 22 MAR 2005
- Manuscript Received: 11 JAN 2005
- Integrative Neural Immune Program (INIP)/National Institute of Mental Health
- cell fusion;
- multiple sclerosis
Membrane cofactor protein (CD46) is a regulator of complement activation that also serves as the entry receptor for human herpes virus 6 (HHV-6) and measles virus (MV) into human cells. While it is clear that oligodendrocytes and astrocytes are cell types commonly infected by these viruses, it is unclear whether oligodendrocytes express CD46, or which are the cellular mechanisms underlying the infection. We show that adult oligodendrocytes, as well as astrocytes and microglial cells, express CD46 on the cellular surface. Moreover, we employed a quantitative fusion assay to demonstrate that HHV-6A infection of T lymphocytes enables cell–cell fusion of these cells to astrocytes or to oligodendroglial cells. This fusion is mediated by the interaction between viral glycoproteins expressed on the membrane of the infected cells and CD46 on the glial targets, and is also observed using cells expressing recombinant MV glycoproteins. These data suggest a mechanism that involves cell–cell fusion by which certain viruses could spread the infection from the periphery to the cells in the nervous system. Published 2005 Wiley-Liss, Inc.