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PDBsum entry 1oop
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Contents |
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271 a.a.
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252 a.a.
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238 a.a.
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58 a.a.
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* Residue conservation analysis
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References listed in PDB file
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Key reference
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Title
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Crystal structure of swine vesicular disease virus and implications for host adaptation.
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Authors
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E.E.Fry,
N.J.Knowles,
J.W.Newman,
G.Wilsden,
Z.Rao,
A.M.King,
D.I.Stuart.
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Ref.
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J Virol, 2003,
77,
5475-5486.
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PubMed id
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Abstract
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Swine vesicular disease virus (SVDV) is an Enterovirus of the family
Picornaviridae that causes symptoms indistinguishable from those of
foot-and-mouth disease virus. Phylogenetic studies suggest that it is a recently
evolved genetic sublineage of the important human pathogen coxsackievirus B5
(CBV5), and in agreement with this, it has been shown to utilize the coxsackie
and adenovirus receptor (CAR) for cell entry. The 3.0-A crystal structure of
strain UK/27/72 SVDV (highly virulent) reveals the expected similarity in core
structure to those of other picornaviruses, showing most similarity to the
closest available structure to CBV5, that of coxsackievirus B3 (CBV3). Features
that help to cement together and rigidify the protein subunits are extended in
this virus, perhaps explaining its extreme tolerance of environmental factors.
Using the large number of capsid sequences available for both SVDV and CBV5, we
have mapped the amino acid substitutions that may have occurred during the
supposed adaptation of SVDV to a new host onto the structure of SVDV and a model
of the SVDV/CAR complex generated by reference to the cryo-electron
microscopy-visualized complex of CBV3 and CAR. The changes fall into three
clusters as follows: one lines the fivefold pore, a second maps to the
CAR-binding site and partially overlaps the site for decay accelerating factor
(DAF) to bind to echovirus 7 (ECHO7), and the third lies close to the fivefold
axis, where the low-density lipoprotein receptor binds to the minor group of
rhinoviruses. Later changes in SVDV (post-1971) map to the first two clusters
and may, by optimizing recognition of a pig CAR and/or DAF homologue, have
improved the adaptation of the virus to pigs.
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