J Virol, June 1998, p. 5245-5250, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Neuropathology Laboratory,
Received 3 November 1997/Accepted 10 March 1998
Measles virus (MV) infection of the human central nervous system
(CNS) typically involves widespread infection of neurons. However,
little is known about how they become infected, how defective virus
arises and accumulates, or how virus spreads among the cells of the
CNS. In vitro studies of viral interactions with human neuronal cells
may contribute to the resolution of such issues. In mixed cultures
containing differentiated human neuronal (hNT2) cells and
neuroepithelial cells, immunofluorescence studies show that the
neurons, unlike both their NT2 progenitors and the neuroepithelial cells, are not initially susceptible to MV infection. This is possibly
due to their lack of expression of CD46, a known cell surface receptor
for MV. Later in the course of infection, however, both MV proteins and
genomic RNA become detectable in their processes, where they contact
infected, fully permissive neuroepithelial cells. Such a mechanism of
virus transfer may be involved in the initiation and spread of
persistent MV infection in diseases such as subacute sclerosing
panencephalitis. Furthermore, mutated defective virus may readily
accumulate and spread without the need, at any stage, for viral
maturation and budding.
*
Corresponding author. Mailing address: Institute of
Pathology, Royal Hospitals Trust, Grosvenor Rd., Belfast BT12 6BL,
Northern Ireland. Phone: 44 1232-240503, ext. 2565. Fax: 44 1232-438024. E-mail: JOHN.KIRK{at}QUB.AC.UK.
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