I'm a biochemist in an unrelated field, but your question piqued my interest, so I went to PubMed while I am waiting on the autoclave. Maybe these can add to the discussion before someone more familiar with rabies sees this thread.

I found a really interesting recent paper about using part of the virus to deliver drugs to the CNS.

Targeted Delivery of Proteins into the Central Nervous System Mediated by Rabies Virus Glycoprotein-Derived Peptide. Fu A, Wang Y, Zhan L, Zhou R. Source School of Pharmaceutical Sciences, Southwest University, Tian Sheng Road, Beibei District, Chongqing, 400716, China, Fuailing1008@hotmail.com.

Abstract PURPOSE: Delivery of therapeutic proteins across the blood-brain barrier (BBB) is severely limited by their size and biochemical properties. Here we showed that a 39-amino acid peptide derived from the rabies virus glycoprotein (RDP) was exploited as an efficient protein carrier for brain-targeting delivery. METHODS: Three proteins with different molecular weight and pI, β-galactosidase (β-Gal), luciferase (Luc) and brain-derived neurotrophic factor (BDNF), were fused to RDP and intravenously injected into the mice respectively. The slices of different tissues with X-Gal staining were used to examine whether RDP could deliver β-Gal targeted into the CNS. The time-course relationship of RDP-Luc was studied to confirm the transport efficiency of RDP. The neuroprotective function of RDP-BDNF was examined in mouse experimental stroke to explore the pharmacological effect of RDP fusion protein. RESULTS: The results showed that the fusion proteins rapidly and specific entered the nerve cells in 15 min, and the t(1/2) was about 1 hr. Furthermore, RDP-BDNF fusion protein showed the neuroprotective properties in mouse experimental stroke including reduction of stroke volume and neural deficit. CONCLUSIONS: RDP provides an effective approach for the targeted delivery of biological active proteins into the central nervous system.

Also, some of the proteins involved in the retrograde transport:

Rabies virus as ribonucleoprotein or whole virion can be transported via retrograde axoplasmic flow from the peripheral inoculation site via peripheral nerves to the CNS. An interaction between P and dynein motor protein via the LC8 binding motif and G protein (in case of whole virion) is required for the transport mechanism. Which mechanism dominates is controversial. The precise steps for G-mediated transport are not known, but neurotrophin p75 NTR may be a factor. G protein can specifically bind to p75 NTR, and ligand p75 NTR complexes are internalized via clathrin-coated pits into early endosomes. They then can move in a retrograde manner.

(Rabies. Hemachudha T, Wacharapluesadee S, Laothamatas J, Wilde H. Curr Neurol Neurosci Rep. 2006 Nov;6(6):460-8. Review.)

Receptors involved.

J Neurovirol. 2005 Feb;11(1):82-7. Rabies virus receptors. Lafon M. Source Unité de Neuroimmunologie Virale, Département de Neuroscience, Institut Pasteur, 75724 Paris cedex 15, France. mlafon@pasteur.fr Abstract

There is convincing in vitro evidence that the muscular form of the nicotinic acetylcholine receptor (nAChR), the neuronal cell adhesion molecule (NCAM), and the p75 neurotrophin receptor (p75NTR) bind rabies virus and/or facilitate rabies virus entry into cells. Other components of the cell membrane, such as gangliosides, may also participate in the entry of rabies virus. However, little is known of the role of these molecules in vivo. This review proposes a speculative model that accounts for the role of these different molecules in entry and trafficking of rabies virus into the nervous system.