These results show, that hedgehogs harbor at least 3 of the 5 recognized Borrelia genospecies found in Germany, all of which are known (B. afzelii, B. garinii) or are strongly suspected (B. spielmanii) of being pathogens for humans (9, 10) . To our knowledge, ours is the fi rst report of B. spielmanii from hedgehogs, a Borrelia sp. that is usually associated with rodents, especially with garden and hazel dormice (10) . That Borrelia spp. infections commonly occur in European hedgehogs is likely. However, questions remain about the role of these pathogens in regulating the populations of European hedgehogs and about the status of these common synanthropic mammals as a reservoir host of B. burgdorferi s. l. in periurban and rural environments. Expression of the VP2 Protein of Murine Norovirus by a Translation Termination-Reinitiation Strategy BACKGROUND: Expression of the minor virion structural protein VP2 of the calicivirus murine norovirus (MNV) is believed to occur by the unusual mechanism of termination codon-dependent reinitiation of translation. In this process, following translation of an upstream open reading frame (ORF) and termination at the stop codon, a proportion of 40S subunits remain associated with the mRNA and reinitiate at the AUG of a downstream ORF, which is typically in close proximity. Consistent with this, the VP2 start codon (AUG) of MNV overlaps the stop codon of the upstream VP1 ORF (UAA) in the pentanucleotide UAA UG. PRINCIPAL FINDINGS: Here, we confirm that MNV VP2 expression is regulated by termination-reinitiation and define the mRNA sequence requirements. Efficient reintiation is dependent upon 43 nt of RNA immediately upstream of the UAA UG site. Chemical and enzymatic probing revealed that the RNA in this region is not highly structured and includes an essential stretch of bases complementary to 18S rRNA helix 26 (Motif 1). The relative position of Motif 1 with respect to the UAA UG site impacts upon the efficiency of the process. Termination-reinitiation in MNV was also found to be relatively insensitive to the initiation inhibitor edeine. CONCLUSIONS: The termination-reinitiation signal of MNV most closely resembles that of influenza BM2. Similar to other viruses that use this strategy, base-pairing between mRNA and rRNA is likely to play a role in tethering the 40S subunit to the mRNA following termination at the VP1 stop codon. Our data also indicate that accurate recognition of the VP2 ORF AUG is not a pre-requisite for efficient reinitiation of translation in this system. For most eukaryotic mRNAs, translation initiation is a 59-enddependent process beginning with recognition of the cap structure by the cap-binding complex eIF4F [1] and (usually) recognition of the AUG codon of the first open reading frame (ORF) on the mRNA by the scanning ribosome complex [2] . This 59-end dependence is a problem faced by many RNA viruses with polycistronic genomes and elaborate strategies have been developed to facilitate access of ribosomes to downstream open reading frames (ORFs). Amongst these, a number of unconventional translation strategies have been described [3] . These include leaky scanning of 40S subunits past the start codon of the first ORF [4] , the possession of intercistronic internal ribosome entry signal [5] , programmed ribosomal frameshifting during elongation [6] and stop codon suppression at the termination step [7] [8] . Another strategy that has evolved to allow expression of a downstream ORF is termination-reinitiation (also referred to here as stop-start). In this process, ribosomes translate the upstream ORF but following termination, a proportion of 40S subunits remain tethered to the mRNA and go on to reinitiate at the start codon of the downstream ORF. This termination-dependent reinitiation strategy allows the coupled expression of products from adjacent ORFs and thus the production of a defined ratio of gene products.