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Journal of Virology, September 2001, p. 8742-8751, Vol. 75, No. 18
Department of Virology, Research Institute
for Microbial Diseases, Osaka University, Suita, Osaka
565-0871,1 and Section of Serology,
Institute of Immunological Science, Hokkaido University, Kita-ku,
Sapporo 060-0815,2 Japan
Received 1 February 2001/Accepted 19 June 2001
The Borna disease virus (BDV) p24 phosphoprotein is an abundant
protein in BDV-infected cultured cells and animal brains. Therefore,
there is a possibility that binding of the p24 protein to cellular
factor(s) induces functional alterations of infected neural cells in
the brain. To identify a cellular protein(s) that interacts with BDV
p24 protein, we performed far-Western blotting with extracts from
various cell lines. Using recombinant p24 protein as a probe, we
detected a 30-kDa protein in all cell lines examined. Binding between
the 30-kDa and BDV p24 proteins was also demonstrated using BDV p24
affinity and ion-exchange chromatography columns. Microsequence
analysis of the purified 30-kDa protein revealed that its N terminus
showed complete homology with rat amphoterin protein, which is a
neurite outgrowth factor abundant in the brain during development.
Mammalian two-hybrid and immunoprecipitation analyses also confirmed
that amphoterin is a specific target for the p24 protein in vivo.
Furthermore, we showed that infection by BDV, as well as purified p24
protein in the medium, significantly decreased cell process outgrowth
of cells grown on laminin, indicating the functional inhibition of
amphoterin by interaction with the p24 protein. Immunohistochemical
analysis revealed decreased levels of amphoterin protein at the leading
edges of BDV-infected cells. Moreover, the expression of the receptor
for advanced glycation end products, of which the extracellular moiety
is a receptor for amphoterin, was not significantly activated in
BDV-infected cells during the process of extension, suggesting that the
secretion of amphoterin from the cell surface is inhibited by the
binding of the p24 protein. These results suggested that BDV infection may cause direct damage in the developing brain by inhibiting the
function of amphoterin due to binding by the p24 phosphoprotein.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.18.8742-8751.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Borna Disease Virus Phosphoprotein Binds a Neurite
Outgrowth Factor, Amphoterin/HMG-1
*
Corresponding author. Mailing address: Department of
Virology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan. Phone: 81-6-6879-8308. Fax: 81-6-6879-8310. E-mail:
tomonaga{at}biken.osaka-u.ac.jp.
Present address: Department of Pathology, National Institute of
Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan.
Journal of Virology, September 2001, p. 8742-8751, Vol. 75, No. 18
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.18.8742-8751.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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