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Journal of Virology, December 2007, p. 13622-13630, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.02368-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Rabies Virus Glycoprotein Receptor p75NTR Is Not Essential for Rabies Virus Infection{triangledown}

Christine Tuffereau,1 Klaus Schmidt,2 Christelle Langevin,1 Florence Lafay,1 Georg Dechant,3 and Martin Koltzenburg2,4*

Laboratoire de Virologie Moléculaire et Structurale, UMR 2472 CNRS-INRA, CNRS, 91198 Gif-sur-Yvette Cedex, France,1 Department of Neurology, University of Würzburg, Würzburg, Germany,2 Department of Neuroscience, University of Innsbruck, Austria,3 UCL Institute of Child Health, University College London, London, United Kingdom4

Received 29 October 2006/ Accepted 1 October 2007

Rabies virus glycoprotein (RVG) is known to be the only factor that mediates rabies infection. The neurotrophin receptor (p75NTR), through its cysteine-rich domain 1, is a specific receptor for RVG and neutralizes virus infectivity, but its role in virus infection has remained obscure. We used adult mouse dorsal root ganglion (DRG) neurons as a model to study the role of p75NTR in RV infection of primary neurons. We show that RV infects around 20% of DRG neurons, of which more than 80% are p75NTR positive, have large diameters, and are capsaicin insensitive. Surprisingly, RV binding and infection are absent in about half of the p75NTR-expressing DRG neurons which have small diameters and are often capsaicin sensitive. This indicates that p75NTR is not sufficient to mediate RV interaction in sensory neurons. The rate and specificity of neural infection are unchanged in RV-infected p75NTRExonIV–/– mice that lack all extracellular receptor domains and in wild-type mice infected with two independent RV mutants that lack p75NTR binding. Accordingly, the mortality rate is unchanged in the absence of RV-p75NTR interaction. We conclude that although p75NTR is a receptor for soluble RVG in transfected cells of heterologous expression systems, an RVG-p75NTR interaction is not necessary for RV infection of primary neurons. This means that other receptors are required to mediate RV infection in vivo and in vitro.

* Corresponding author. Mailing address: UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom. Phone: 44 (20) 7905 2701. Fax: 44 (20) 7905 2702. E-mail: M.Koltzenburg{at}ich.ucl.ac.uk

{triangledown} Published ahead of print on 10 October 2007.

Journal of Virology, December 2007, p. 13622-13630, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.02368-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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