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Journal of Virology, May 2009, p. 4995-5004, Vol. 83, No. 10
0022-538X/09/$08.00+0     doi:10.1128/JVI.02225-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Receptor-Dependent and -Independent Axonal Retrograde Transport of Poliovirus in Motor Neurons{triangledown} ,{dagger}

Seii Ohka,1* Mai Sakai,1 Stephanie Bohnert,2 Hiroko Igarashi,1 Katrin Deinhardt,2,{ddagger} Giampietro Schiavo,2 and Akio Nomoto1

Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan,1 Molecular NeuroPathobiology Laboratory, Cancer Research UK London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, United Kingdom2

Received 22 October 2008/ Accepted 18 February 2009

Poliovirus (PV), when injected intramuscularly into the calf, is incorporated into the sciatic nerve and causes an initial paralysis of the inoculated limb in transgenic (Tg) mice carrying the human PV receptor (hPVR/CD155) gene. We have previously demonstrated that a fast retrograde axonal transport process is required for PV dissemination through the sciatic nerves of hPVR-Tg mice and that intramuscularly inoculated PV causes paralytic disease in an hPVR-dependent manner. Here we showed that hPVR-independent axonal transport of PV was observed in hPVR-Tg and non-Tg mice, indicating that several different pathways for PV axonal transport exist in these mice. Using primary motor neurons (MNs) isolated from these mice or rats, we demonstrated that the axonal transport of PV requires several kinetically different motor machineries and that fast transport relies on a system involving cytoplasmic dynein. Unexpectedly, the hPVR-independent axonal transport of PV was not observed in cultured MNs. Thus, PV transport machineries in cultured MNs and in vivo differ in their hPVR requirements. These results suggest that the axonal trafficking of PV is carried out by several distinct pathways and that MNs in culture and in the sciatic nerve in situ are intrinsically different in the uptake and axonal transport of PV.

* Corresponding author. Mailing address: Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. Phone: 81-3-5841-3407. Fax: 81-3-5841-3374. E-mail: seii{at}m.u-tokyo.ac.jp

{triangledown} Published ahead of print on 25 February 2009.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} Present address: Molecular Neurobiology Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016.

Journal of Virology, May 2009, p. 4995-5004, Vol. 83, No. 10
0022-538X/09/$08.00+0     doi:10.1128/JVI.02225-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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