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Title: Infection of the enteric nervous system by Borna Disease Virus (BDV) upregulates expression of Calbindin D-28k

Author
item PFANNKUCHE, HELGA - LEIPZIG UNIVERSITY
item KONRATH, ANDREA - LEIPZIG UNIVERSITY
item BUCHHOLZ, INGEBORG - LEIPZIG UNIVERSITY
item Richt, Juergen
item SEEGER, JOHANNES - LEIPZIG UNIVERSITY
item MULLER, HERMANN - LEIPZIG UNIVERSITY
item GABEL, GOTTHOLD - LEIPZIG UNIVERSITY

Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/11/2007
Publication Date: 3/18/2008
Citation: Pfannkuche, H., Konrath, A., Buchholz, I., Richt, J.A., Seeger, J., Muller, H., Gabel, G. 2008. Infection of the enteric nervous system by Borna Disease Virus (BDV) upregulates expression of Calbindin D-28k. Veterinary Microbiology. 127(3-4):275-285.

Interpretive Summary: Borna disease virus (BDV) causes a persistent infection of the central nervous system associated with non-protective immune responses. Borna disease is actually caused by side effects of the immune response to the viral infection, not by the virus itself. BDV can infect a wide range of warm-blooded animals with horses and sheep being the main natural hosts; there is speculation that BDV can also infect humans. This work, in a rat model of Borna disease, describes that BDV can also infect neurons of the enteric nervous system. This study offers an explanation for the fact that horses infected with BDV show dysfunctions of the GI-tract beside neurological symptoms.

Technical Abstract: Borna disease virus (BDV) is a neurotropic agent infecting distinct neuronal subpopulations in the central nervous system of various mammalian species likely including humans. Horses, a major natural host for BDV, show dysfunctions of the gastrointestinal tract beside characteristic neurological symptoms. Therefore, we hypothesized that the enteric nervous system (ENS) may be a target of BDV replication. The presence of BDV-specific antigen in subpopulations of the ENS was investigated. Four-week-old Lewis rats were infected intracerebrally and sacrificed 4 to 14 weeks post infection (p.i.). BDV-immunoreactive neurons were found in submucosal and myenteric neurons of the proximal colon. Fourteen weeks p.i., the proportion of BDV-positive neurons was 44 equal to or greater than 17% and 24 equal to or greater than 7% in the submucous and myenteric plexus, respectively. The majority of BDV-positive myenteric neurons showed immunoreactivity for choline acetyltransferase. Expression of Calbindin D-28k (CALB) was found in 96% of submucosal and in 67% of myenteric BDV40 immunoreactive neurons. Additionally, the number of CALB-immunoreactive neurons was significantly higher in the myenteric plexus of infected rats compared to controls. These data indicate that BDV infects specific subpopulations of enteric neurons. Therefore the ENS might serve as a site for BDV replication and as an immunoprivileged reservoir for BDV. In addition, upregulation of CALB in neurons of the myenteric plexus is probably induced during BDV-infection.