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J Virol, August 1998, p. 6511-6519, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Involvement of Aminopeptidase N (CD13) in Infection of Human Neural Cells by Human Coronavirus 229E

Claude Lachance,1 Nathalie Arbour,1 Neil R. Cashman,2 and Pierre J. Talbot1,*

Laboratory of Neuroimmunovirology, Armand-Frappier Institute, University of Quebec, Laval, Quebec H7V 1B7,1 and Montreal Neurological Institute and Hospital, Montreal, Quebec H3A 2B4,2 Canada

Received 19 February 1998/Accepted 11 May 1998

Attachment to a cell surface receptor can be a major determinant of virus tropism. Previous studies have shown that human respiratory coronavirus HCV-229E uses human aminopeptidase N (hAPN [CD13]) as its cellular receptor for infection of lung fibroblasts. Although human coronaviruses are recognized respiratory pathogens, occasional reports have suggested their possible neurotropism. We have previously shown that human neural cells, including glial cells in primary cultures, are susceptible to human coronavirus infection in vitro (A. Bonavia, N. Arbour, V. W. Yong, and P. J. Talbot, J. Virol. 71:800-806, 1997). However, the only reported expression of hAPN in the nervous system is at the level of nerve synapses. Therefore, we asked whether hAPN is utilized as a cellular receptor for infection of these human neural cell lines. Using flow cytometry, we were able to show the expression of hAPN on the surfaces of various human neuronal and glial cell lines that are susceptible to HCV-229E infection. An hAPN-specific monoclonal antibody (WM15), but not control antibody, inhibited the attachment of radiolabeled HCV-229E to astrocytic, neuronal, and oligodendrocytic cell lines. A correlation between the apparent amount of cell surface hAPN and the level of virus attachment was observed. Furthermore, the presence of WM15 inhibited virus infection of these cell lines, as detected by indirect immunofluorescence. These results indicate that hAPN (CD13) is expressed on neuronal and glial cell lines in vitro and serves as the receptor for infection by HCV-229E. This further strengthens the neurotropic potential of this human respiratory virus.

* Corresponding author. Mailing address: Laboratoire de neuroimmunovirologie, Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec, Canada H7V 1B7. Phone: (514) 687-5010, ext. 4406. Fax: (514) 686-5531 (or 5626). E-mail: Pierre.Talbot{at}iaf.uquebec.ca.

J Virol, August 1998, p. 6511-6519, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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