Serological Relationship of Swine Vesicular Disease Virus and Coxsackie B5 Virus

Nature ◽  
1973 ◽  
Vol 245 (5424) ◽  
pp. 314-315 ◽  
Author(s):  
J. H. GRAVES
Keyword(s):  
Disease Virus ◽  
Serological Relationship ◽  
Swine Vesicular Disease Virus ◽  
Relationship Of ◽  
Vesicular Disease

scholarly journals Importance of Arginine 20 of the Swine Vesicular Disease Virus 2A Protease for Activity and Virulence

2005 ◽  
Vol 79 (1) ◽  
pp. 428-440 ◽  
Author(s):  
Toru Inoue ◽  
Soren Alexandersen ◽  
Angela T. Clark ◽  
Ciara Murphy ◽  
Melvyn Quan ◽  
...  
Keyword(s):  
Disease Virus ◽  
Direct Sequencing ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Internal Ribosome Entry ◽  
Virus Growth ◽  
Swine Vesicular Disease Virus ◽  
2A Protease ◽  
Viral Polyprotein ◽  
Vesicular Disease

ABSTRACT A major virulence determinant of swine vesicular disease virus (SVDV), an Enterovirus that causes an acute vesicular disease, has been mapped to residue 20 of the 2A protease. The SVDV 2A protease cleaves the 1D-2A junction in the viral polyprotein, induces cleavage of translation initiation factor eIF4GI, and stimulates the activity of enterovirus internal ribosome entry sites (IRESs). The 2A protease from an attenuated strain of SVDV (Ile at residue 20) is significantly defective at inducing cleavage of eIF4GI and the activation of IRES-dependent translation compared to the 2A protease from a pathogenic strain (J1/73, Arg at residue 20), but the two proteases have similar 1D-2A cleavage activities (Y. Sakoda, N. Ross-Smith, T. Inoue, and G. J. Belsham, J. Virol. 75:10643-10650, 2001). Residue 20 has now been modified to every possible amino acid, and the activities of each mutant 2A protease has been analyzed. Selected mutants were reconstructed into full-length SVDV cDNA, and viruses were rescued. The rate of virus growth in cultured swine kidney cells reflected the efficiency of 2A protease activity. In experimentally infected pigs, all four of the mutant viruses tested displayed much-reduced virulence compared to the J1/73 virus but a significant, albeit reduced, level of viral replication and excretion was detected. Direct sequencing of cDNA derived from samples taken early and late in infection indicated that a gradual selection-reversion to a more efficient protease occurred. The data indicated that extensive sequence change and selection may introduce a severe bottleneck in virus replication, leading to a decreased viral load and reduced or no clinical disease.

Molecular cloning, expression and immunological analysis of the capsid precursor polypeptide (P1) from swine vesicular disease virus

1998 ◽  
Vol 57 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Miguel A Jiménez-Clavero ◽  
Estela Escribano-Romero ◽  
José M Sánchez-Vizcaı́no ◽  
Victoria Ley
Keyword(s):  
Molecular Cloning ◽  
Disease Virus ◽  
Immunological Analysis ◽  
Capsid Precursor ◽  
Swine Vesicular Disease Virus ◽  
Vesicular Disease

scholarly journals More recent swine vesicular disease virus isolates retain binding to coxsackie–adenovirus receptor, but have lost the ability to bind human decay-accelerating factor (CD55)

2005 ◽  
Vol 86 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
Miguel A. Jimenez-Clavero ◽  
Estela Escribano-Romero ◽  
Victoria Ley ◽  
O. Brad Spiller
Keyword(s):  
Cell Line ◽  
Disease Virus ◽  
Hela Cells ◽  
Virus Titre ◽  
Decay Accelerating Factor ◽  
Coxsackie Adenovirus Receptor ◽  
Swine Vesicular Disease Virus ◽  
Virus Serotype ◽  
Adenovirus Receptor ◽  
Vesicular Disease

Swine vesicular disease virus (SVDV) evolved from coxsackie B virus serotype 5 (CVB5) in the recent past, crossing the species barrier from humans to pigs. Here, SVDV isolates from early and recent outbreaks have been compared for their capacity to utilize the progenitor virus receptors coxsackie–adenovirus receptor (CAR) and decay-accelerating factor (DAF; CD55). Virus titre of CVB5 and SVDV isolates It′66 and UK′72 on human HeLa cells was reduced by pre-incubation with either anti-DAF or anti-CAR antibodies; however, recent SVDV isolates R1072, R1120 and SPA′93 did not infect HeLa cells lytically. CVB5 and SVDV infection of the pig cell line IB-RS-2 was inhibited completely by anti-CAR antibodies for all isolates, and no reduction was observed following pre-incubation of cells with anti-pig DAF antibodies. Expression of human DAF in the pig cell line IB-RS-2 enhanced the virus titre of early SVDV isolates by 25-fold, but had no effect on recent SVDV isolate titre. Binding of radiolabelled CVB5 to IB-RS-2 cells was increased seven- to eightfold by expression of human DAF and binding of early SVDV isolates was increased 1·2–1·3-fold, whereas no increase in binding by recent SVDV isolates was mediated by human DAF expression. Addition of soluble hDAF-Fc inhibited CVB5, but not SVDV, infection of pig cells. Pre-incubation of all viruses with soluble hCAR-Fc blocked infection of IB-RS-2 pig cells completely; titration of the amount of soluble hCAR-Fc required to block infection revealed that early isolate UK′72 was the least susceptible to inhibition, and the most recent isolate, SPA′93, was the most susceptible.

scholarly journals The airborne excretion by pigs of swine vesicular disease virus

1974 ◽  
Vol 72 (1) ◽  
pp. 61-65 ◽  
Author(s):  
R. F. Sellers ◽  
K. A. J. Herniman
Keyword(s):  
Respiratory Tract ◽  
Disease Virus ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Swine Vesicular Disease Virus ◽  
Foot And Mouth ◽  
Vesicular Disease

SUMMARYThe air of loose-boxes holding pigs affected with swine vesicular disease was sampled for virus. In the multistage impinger virus to a titre of 102·6TCID50 was associated with particles greater than 6 μm., 101·6with particles 3–6 μm. and 101·4or less with particles less than 3 μm. In the noses of workers in contact with the pigs for periods not less than 5 min., virus to a titre of 102·4TCID50 was found. Virus was recovered from the air for 2–3 days during the disease and maximum titre in pigs infected by injection or by contact occurred on the second to third day after generalization of the lesions. The amounts of virus were about 160-fold less than those recovered from pigs affected with foot-and-mouth disease, and the quantity and time of excretion suggest that the source of swine vesicular disease virus in the aerosol may be from the lesions and skin rather than from the respiratory tract.

Use of Oral Fluids for Detection of Virus and Antibodies in Pigs Infected with Swine Vesicular Disease Virus

2016 ◽  
Vol 64 (6) ◽  
pp. 1762-1770 ◽  
Author(s):  
C. Senthilkumaran ◽  
H. Bittner ◽  
A. Ambagala ◽  
O. Lung ◽  
S. Babiuk ◽  
...  
Keyword(s):  
Disease Virus ◽  
Oral Fluids ◽  
Swine Vesicular Disease Virus ◽  
Vesicular Disease

118. Detection and quantification of swine vesicular disease virus by TaqMan® RT-PCR assay

2003 ◽  
Vol 74 ◽  
pp. 40
Author(s):  
S.M. Reid ◽  
D.J. Paton ◽  
G. Wilsden ◽  
G.H. Hutchings ◽  
S. Alexandersen
Keyword(s):  
Disease Virus ◽  
Rt Pcr ◽  
Pcr Assay ◽  
Swine Vesicular Disease Virus ◽  
Vesicular Disease ◽  
Detection And Quantification

Chemical Inactivation of Swine Vesicular Disease Virus

1975 ◽  
Vol 131 (3) ◽  
pp. 317-323 ◽  
Author(s):  
J.H. Blackwell ◽  
J.H. Graves ◽  
P.D. McKercher
Keyword(s):  
Disease Virus ◽  
Chemical Inactivation ◽  
Swine Vesicular Disease Virus ◽  
Vesicular Disease

scholarly journals Near-Complete Genome Sequencing of Swine Vesicular Disease Virus Using the Roche GS FLX Sequencing Platform

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97180 ◽  
Author(s):  
Sandra C. Abel Nielsen ◽  
Christian A. W. Bruhn ◽  
Jose Alfredo Samaniego ◽  
Jemma Wadsworth ◽  
Nick J. Knowles ◽  
...  
Keyword(s):  
Disease Virus ◽  
Genome Sequencing ◽  
Complete Genome ◽  
Sequencing Platform ◽  
Complete Genome Sequencing ◽  
Swine Vesicular Disease Virus ◽  
Vesicular Disease
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