Arch Virol (2003) 148: 1747–1756
Effects of mutations in the VP2/VP4 cleavage
site of Swine vesicular disease virus on RNA
encapsidation and viral infectivity
J. M. J. Rebel, C. H. Leendertse, A. Dekker, and R. J. M. Moormann
Institute of Animal Science and Health, ID-Lelystad, Lelystad, Netherlands
Received August 12, 2002; accepted March 28, 2003
Published online June 5, 2003
Summary. We studied VP0 cleavage of Swine vesicular disease virus (SVDV), a
member of the Picornaviridae using a full-length cDNA copy of the Dutch SVDV
isolate. The inﬂuences of mutations, introduced at the cleavage site of SVDV, on
VP0 cleavage, RNA encapsidation and viral infection were studied.
Double mutations at asparagine (VP0 aa 69) and serine (VP0 aa 70) resulted
in no cleavage of VP0 and 100% inhibition of virus production. Mutation of the
asparagine into threonine or phenylalanine resulted in a low amount of cleavedVP0
and infectious virus was found. After passage of this mutated virus VP0 cleavage
became more efﬁcient and the growth rate of the virus became similar to wild-type
SVDV. The passaged virus had mutated at the asparagine site; the threonine had
changed into an alanine and the phenylalanine into a cysteine. When the serine
was mutated no maturation cleavage was observed and no infectious virus could
be derived. All the mutations resulted in RNA encapsidation. We conclude that
in the case of SVDV the cleavage site between VP2 and VP4 is essential for the
formation of infectious virus which is comparable to poliovirus. The serine of the
VP0 site was more important than the asparagine in this respect.
Swine vesicular disease virus (SVDV) is the causative agent of a highly contagious
disease in pigs, which causes vesicular lesions in the mouth and on the feet.
Symptoms are clinically indistinguishable from those caused by Foot-and-mouth
disease virus and SVD is therefore classiﬁed as a list A disease by the ofﬁce
international des epizooties (OIE). The virus was for the ﬁrst time observed in
Italy in 1966  and since then more outbreaks in Europe and Asia did occur .
SVDV is classiﬁed in genus Enterovirus within the family Picornaviridae. The
virus is non-enveloped and has a 30 nm capsid of icosahedral symmetry, which