Arch Virol (1997) 142: 2035±2042
Amantadine does not have antiviral activity
against Borna disease virus
B. Cubitt and J. C. de la Torre
Division of Virology, Department of Neuropharmacology,
The Scripps Research Institute, La Jolla, California U.S.A.
Accepted June 19, 1997
Summary. We have investigated the antiviral activity of amantadine (AD)
against Borna disease virus (BDV) in several culture cell systems. We present
evidence that AD, in the range 5 to 10 mM, does not have antiviral activity
against BDV. Treatment of BDV infected cells with AD for six days caused
neither a reduction in the number of infected cells, nor a decrease in steady state
levels of BDV RNA or proteins. Moreover, treatment of cells with AD prior
infection did not affect BDV multiplication, whereas in¯uenza A virus yield
was less than 1% with respect to that obtained in untreated control cells.
Borna disease virus (BDV) causes CNS disease in several vertebrate species
which is characterized by behavioral abnormalities . BDV has a non-
segmented, negative-stranded (NNS) RNA genome with an organization
characteristic of Mononegavirales [5, 6, 9, 23]. However, BDV differs from
all other known NNS RNA animal viruses in several aspects, including a
nuclear site for the replication and transcription of its genome [4, 8], and the use
of host cellular RNA splicing machinery for the regulation of its gene
expression [7, 24]. Based on its unique features, BDV has been proposed to be
the prototype of a new virus family, Bornaviridae [9, 23].
There is a body of evidence to indicate that viral brain infection represents
an important risk factor in schizophrenia and affective disorders [20a, 29].
Seroepidemiological data [1, 20, 27], together with recent molecular epi-
demiological studies [2, 10, 15, 22], and the detection of BDV RNA and antigen
in autopsy brain cases from patients who presented with severe depression and
memory loss , support that BDV infection is associated with certain