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Borna disease virus 1 (BoDV-1) causes encephalitis with a fatality rate of > 90% in domestic mammals and humans. Currently, the bicolored white-toothed shrew is the only known reservoir host.
We report BoDV-1 infections in 15 wild European hedgehogs from an endemic area in Germany. Because hedgehogs are distant relatives of shrews and often cared for by humans, the cases raise concern regarding a potential zoonotic risk.
All the hedgehogs that tested positive for BoDV-1 died of neurological disease and exhibited severe polio-predominant lymphoplasmohistiocytic meningoencephalitis. However, because of the detection of viral antigens in nonneural cells in 1 animal, we cannot completely exclude that some infected hedgehogs shed the virus.
Although direct BoDV-1 transmission is known to be inefficient, our results emphasize the necessity of hygiene measures when handling hedgehogs, especially those with neurological signs who are from BoDV-1–endemic regions.
Borna disease virus 1 (BoDV-1; Orthobornavirus bornaense, family Bornaviridae) is an established cause of severe immune-mediated meningoencephalitis across parts of central Europe and has been recognized to produce high case-fatality rates in domestic mammals and in humans.
The virus’s recognized natural reservoir is the insectivorous bicolored white-toothed shrew (Crocidura leucodon), which carries persistent infection with widespread tissue distribution and continuous viral shedding without apparent disease.
Prior to the present report, hedgehogs (Erinaceus europaeus), although insectivorous and in frequent contact with humans during rehabilitation, had not been documented as BoDV-1 hosts.
The present source reports detection of BoDV-1 infection and associated fatal neuroinflammatory disease in wild European hedgehogs originating from a known BoDV-1–endemic region in Bavaria, Germany, with first detection in 2022 and subsequent clustered detections in 2024–2025.
The authors sought to characterize BoDV-1 infection in hedgehogs found with nonsuppurative encephalitis and to evaluate tissue distribution, cell tropism, pathology, and molecular phylogeny of virus sequences recovered.
The investigation included a case series of hedgehogs that died or were euthanized because of histopathologically diagnosed nonsuppurative encephalitis, paired with a contemporaneous control series of nonencephalitic hedgehogs from the same geographic region.
Inclusion was based on postmortem diagnosis of lymphoplasmohistiocytic meningoencephalitis.
For BoDV-1–positive animals, IHC for BoDV-1 nucleoprotein (antibody Bo18) and RNAscope in situ hybridization (ISH) targeting viral RNA encoding matrix protein and glycoprotein (genome positions 2,236–3,747; probe V-BoDV1-G) were applied to CNS and selected peripheral tissues.
Select CNS and peripheral tissues from one case (case 5) were additionally tested with a rabbit anti–BoDV-1 nucleoprotein polyclonal serum.
Sequences were deposited in GenBank and used in phylogenetic analysis.
None of the 33 nonencephalitic control hedgehogs tested positive for BoDV-1 RNA.
Clinical signs reported by submitters included incoordination, gait abnormalities, seizures, apathy, spontaneous muscle twitching, impaired thermoregulation, and vestibular manifestations including unilateral head tilt.
The timing of symptom onset relative to discovery varied: most animals had neurologic signs at presentation, one animal developed neurologic manifestations after 15 days in care, and another had been in rehabilitation and hibernated before neurologic signs appeared months later.
Survival time in care ranged up to 58 days before death or euthanasia.
Specific gross pathology findings were not summarized in detail in the provided source content.
Phenotyping IHC characterized the inflammatory infiltrate (markers CD3, Pax5, Iba1) and demonstrated astrocytic response via GFAP staining.
Specific regional distributions within the CNS and quantification of inflammatory cell types were not provided in the excerpt beyond the overall pattern described.
In one animal, viral antigen was identified in nonneural cells, indicating that tissue distribution may not be strictly limited to neural tissue in every case; the source explicitly stated that this finding prevents complete exclusion of potential viral shedding from some infected hedgehogs.
Nonetheless, the typical pattern described for dead-end hosts (predominant neurotropism without detectable shedding) in other species was noted as the prevailing paradigm, and the detection of antigen in nonneural cells was highlighted as an exception warranting caution.
Hedgehogs are taxonomically distant but insectivorous and may share ecological niches with shrews.
The finding of viral antigen in nonneural cells in one hedgehog led the authors to note that viral shedding by some infected hedgehogs cannot be entirely ruled out.
Thus direct evidence for hedgehog-to-human or hedgehog-to-animal transmission, or routine shedding patterns in hedgehogs, was not established in the presented material.
The established reservoir remains the bicolored white-toothed shrew.
The reported cases alone do not fulfill reservoir host criteria (e.g., persistent infection with shedding in a clinically inapparent state).
They underscore that the inability to exclude shedding in at least one case motivates a precautionary approach among handlers and rehabilitation personnel.
This report documents a series of fatal BoDV-1–associated meningoencephalitis cases in wild European hedgehogs from a BoDV-1–endemic region in Bavaria, confirmed by qRT-PCR, IHC, and RNAscope ISH, and characterized by severe lymphoplasmohistiocytic polioencephalitic inflammation.
All BoDV-1–positive hedgehogs in the series died or were euthanized following progressive neurologic illness.
The finding of viral antigen in nonneural cells in one animal introduces uncertainty regarding potential viral shedding from hedgehogs and supports the need for hygienic precautions during handling.
The investigation did not identify BoDV-1 RNA in nonencephalitic control hedgehogs included in the sampled cohort.
The established reservoir for BoDV-1 remains the bicolored white-toothed shrew; these hedgehog data document spillover-associated disease rather than established reservoir status.
Several critical gaps remain, including systematic evaluation of shedding, the extent of hedgehog exposure within endemic regions, and detailed phylogenetic inferences connecting hedgehog viruses to local reservoir strains—areas that ongoing and future work will need to address.