Naslov
Borna Disease Virus infects human primary neural stem cells and impairs neurogenesis

Autori
Brnic, Dragan ; Agier, Cécilia ; Eloit, Marc ; Coulpier, Muriel

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Journal of Neurovirology / Khalili, Kamel - Milano : Springer, 2010, 29-29

Skup
10th International Symposium on NeuroVirology

Mjesto i datum
Milano, Italija, 12.10.2010. - 16.10.2010

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Borna Disease Virus; Human Neural Stem Cells; Neurogenesis
(borna disease virus; human neural stem cells; neurogenesis)

Sažetak
Borna disease Virus (BDV) is a non-segmented, negative-strand RNA virus, capable of infecting a large number of vertebrates. In mammals, persistent infection of the central nervous system (CNS) leads to behavioural disorders. BDV is a recognized pathogen in veterinarian field but it also infects humans and might be involved in mental diseases, such as schizophrenia. Neurogenic niches such as the subventricular zone and the sugranular zone of the dentate gyrus as well as neural progenitors cells have been shown to be infected by BDV in experimentally infected rats and it was suggested that neural progenitors might be involved in BDV-induced pathogenesis. Interestingly, there has been argument lately in favour of a role for hippocampal neural stem cells in the neurophysiopathology of schizophrenia. The aim of our study was to investigate whether primary human neural stem cells (hNSC)are permissive to BDV and whether BDV might alter the physiology of these cells. Human primary NSC cultures were established from the CNS of human embryos. We demonstrated that they are highly permissive to the viral BDV strain He80, isolated from a diseased horse. BDV-He80 productively replicates and disseminates in hNSC. The morphology, survival and nestin expression were not altered in BDV-infected NSC although the virus persists for at least 12 passages. On the contrary, BDV strongly impaired neurogenesis when differentiation was induced by withdrawal of growth factors. Both, a decrease in the number of newly formed neurons and a decrease in their survival was observed. This was specific to neurogenesis since astrogliosis was not altered. In conclusion, we provide evidence that BDV is capable of damaging human neurogenesis and we demonstrate a new mechanism by which BDV might impair neural function in infected individuals. These results may help to understand the behavioural disorders associated with BDV infection.

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti

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