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Journal of General Virology (1995), 76, 729-740. Printed in Great Brita& 729
A set of African swine fever virus tandem repeats shares similarities with
SAR-like sequences
F. Almazfin, J. R. Murgnia, J. M. Rodriguez, I. de la Vega and E. Vifiuela*
Centro de Biologia Molecular "Severo Ochoa' ( CSIC-UAM ), Facultad de Ciencias, Universidad Autrnoma,
Cantoblanco, 28049 Madrid, Spain
A group of cross-hybridizing DNA segments contained
within the EcoRI restriction fragments U', X and J of a
Vero cell-adapted strain (BA71V) of African swine fever
virus (ASFV) were mapped and sequenced. Analysis of
the nucleotide sequence revealed the presence of a set of
long internal repeated sequences composed of five types
of tandemly repeat units of about 200 bp. These tandem
repeats contain a G-rich core of 10-14 nucleotides
surrounded by regions with a high A+T content
distributed in oligo(dA), oligo(dT) tracts. Next to the
repeated sequences we detected two related open
reading frames that are members of a new multigene
family (multigene family 300). Comparison of DNA
sequences from several virus isolates indicated that this
region undergoes frequent rearrangements leading to
either duplications or deletions of the repeat units.
These ASFV repeated sequences share similarities with
chromosomal ~ satellite DNA, the scaffold-associated
region and satellite III of Drosophila. Similar tandemly
repeated sequences have not been described in other
viruses.
Introduction
African swine fever virus (ASFV), a large enveloped
icosahedral deoxyvirus, is the causative agent of an
important disease of domestic pigs and related species of
the Suidae family (reviewed in Vifiuela, 1987; Costa,
1990). Unfortunately, although a number of strategies
have been explored including immunization with inacti-
vated virus particles, inoculation with attenuated ASFV
strains and immunization with different purified virus
polypeptides, reliable protection against ASFV has never
been achieved (Wardley et al., 1987; Escribano et al.,
1993). The difficulties encountered in the search for an
ASFV vaccine along with the proficiency of the virus to
establish persistent infections have led to speculation
that ASFV might use mechanisms to counteract the host
immune defences.
The ASFV genome is a single molecule of double-
stranded DNA of approximately 170 kb, with covalently
linked ends (Ortin et al., 1979) and terminal inverted
repetitions (TIR) (Sogo et al., 1984; de la Vega et al.,
1994) similar to those of poxviruses (Wittek & Moss,
* Author for correspondence. Fax + 34 1 3974799. e-mail
FALMAZAN@MVAX.CBM.UAM.ES
The nucleotide sequence data reported have been deposited in
GenBank under accessionnumber U13763,
1980; Baroudy et al., 1982). Crosslinks are composed of
partially unpaired and A-T-rich sequences that are
found as flip-flop forms at the DNA ends (Gonzfilez et
al., 1986). Also in common with the poxviruses (Moss,
1990), ASFV particles contain the enzymic machinery
required for the synthesis of mature virus early mRNAs
(Kuznar et al., 1980; Salas et al., 1981, 1986).
Two types of internal repetitions have been described
within the genome of ASFV: long (over 200 bp) repeats
associated with multigene families located next to the
TIR at both ends of the virus genome; and short
(10-50bp) repeats detected in both intergenic and
intragenic regions. So far, four multigene families have
been described and analysed in detail. Multigene families
110 (Almendral et al., 1990), 360 (Gonz~ilez et al., 1990)
and 505 (Rodr~guez et al., 1994) were initially detected in
the BA71V strain of ASFV; multigene family 100 was
first identified in the virulent strain Malawi LIL20/1
(Vydelingum et al., 1993). Genetic variation in ASFV
DNA takes place mainly through deletion or addition of
DNA sequences in regions located close to the genome
ends (Dixon & Wilkinson, 1988; Blasco et al., 1989a).
The main variation detected when comparing different
virus field isolates is a change in the number of genes
belonging to multigene families. Additionally, new genes
can be generated by recombination events between
homologous genes (Blasco et al., 1989 b; de la Vega et al.,
1990; Dixon et al., 1993). Nothing is known about the
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