Bornaviruses, which chronically infect many species, can cause severe
neurological diseases in some animal species; their association with human
neuropsychiatric disorders is, however, debatable. The epidemiology of Borna
disease virus (BDV), as for other members of the family
Bornaviridae, is largely unknown, although evidence exists
for a reservoir in small mammals, for example bank voles (Myodes
glareolus). In addition to the current exogenous infections and
despite the fact that bornaviruses have an RNA genome, bornavirus sequences
integrated into the genomes of several vertebrates millions of years ago. Our
hypothesis is that the bank vole, a common wild rodent species in traditional
BDV-endemic areas, can serve as a viral host; we therefore explored whether this
species can be infected with BDV, and if so, how the virus spreads and whether
viral RNA is transcribed into DNA in vivo.We infected neonate bank voles intracerebrally with BDV and euthanized them 2 to
8 weeks post-infection. Specific Ig antibodies were detectable in 41%.
Histological evaluation revealed no significant pathological alterations, but
BDV RNA and antigen were detectable in all infected brains. Immunohistology
demonstrated centrifugal spread throughout the nervous tissue, because viral
antigen was widespread in peripheral nerves and ganglia, including the
mediastinum, esophagus, and urinary bladder. This was associated with viral
shedding in feces, of which 54% were BDV RNA-positive, and urine at
17%. BDV nucleocapsid gene DNA occurred in 66% of the infected
voles, and, surprisingly, occasionally also phosphoprotein DNA. Thus,
intracerebral BDV infection of bank vole led to systemic infection of the
nervous tissue and viral excretion, as well as frequent reverse transcription of
the BDV genome, enabling genomic integration. This first experimental bornavirus
infection in wild mammals confirms the recent findings regarding bornavirus DNA,
and suggests that bank voles are capable of bornavirus transmission.