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First published online 19 October 2004
doi: 10.1242/jcs.01484

Journal of Cell Science 117, 5591-5597 (2004)
Published by The Company of Biologists 2004
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Research Article

Inhibition of PrPSc formation by lentiviral gene transfer of PrP containing dominant negative mutations

Carole Crozet1, Yea-Lih Lin2, Clément Mettling2, Chantal Mourton-Gilles3, Pierre Corbeau2, Sylvain Lehmann1,4 and Véronique Perrier1,*

1 Laboratoire de Biologie des Encéphalopathies Spongiformes, CNRS UPR 1142, 141 rue de la Cardonille, 34396 Montpellier CEDEX 5, France
2 Laboratoire Lentivirus et Transfert de Gènes – Institut de Génétique Humaine, CNRS UPR 1142, 141 rue de la Cardonille, 34396 Montpellier CEDEX 5, France
3 BIO-RAD, Centre de Pharmacologie et Biotechnologies pour la Santé, CNRS UMR 5094, 15 avenue C. Flahault, 34060 Montpellier CEDEX 2, France
4 Laboratoire de Biochimie. Hopital St Eloi, 80 avenue A. Fliche 34295 Montpellier CEDEX 5, France

* Author for correspondence (e-mail: vperrier{at}igh.cnrs.fr)

Accepted 21 July 2004

Currently, there is no treatment to cure transmissible spongiform encephalopathies. By taking advantage of the `prion-resistant' polymorphisms Q171R and E219K that naturally exist in sheep and humans, respectively, we have evaluated a therapeutic approach of lentiviral gene transfer. Here, we show that VSV-G (vesicular stomatitis virus G glycoprotein) pseudotyped FIV-(feline immunodeficiency virus) derived vectors carrying the mouse Prnp gene in which these mutations have been inserted, are able to inhibit prion replication in chronically prion-infected cells. Because lentiviral tools are able to transduce post-mitotic cells such as neurons or cells of the lymphoreticular system, this result might help the development of gene- or cell-therapy approaches to prion disease.

Key words: PrP, Prion, Dominant negative, Lentivirus, Therapy


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JCS 2004 117: 2303. [Full Text]  



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© The Company of Biologists Ltd 2004