scholarly journals Heat inactivation of foot-and-mouth disease virus, swine vesicular disease virus and classical swine fever virus when air-dried on plastic and glass surfaces

2021 ◽  
Author(s):  
Thea Kristensen ◽  
Graham J. Belsham ◽  
Kirsten Tjørnehøj
Keyword(s):  
Disease Virus ◽  
Classical Swine Fever Virus ◽  
Foot And Mouth Disease ◽  
Classical Swine Fever ◽  
Mouth Disease ◽  
Heat Inactivation ◽  
Swine Vesicular Disease Virus ◽  
Mouth Disease Virus ◽  
Glass Surfaces ◽  
Vesicular Disease

scholarly journals Dynamics of picornavirus RNA replication within infected cells

2008 ◽  
Vol 89 (2) ◽  
pp. 485-493 ◽  
Author(s):  
Graham J. Belsham ◽  
Preben Normann
Keyword(s):  
Disease Virus ◽  
Rna Synthesis ◽  
Foot And Mouth Disease ◽  
Rna Replication ◽  
Mouth Disease ◽  
Swine Vesicular Disease Virus ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Infected Cells ◽  
Vesicular Disease

Replication of many picornaviruses is inhibited by low concentrations of guanidine. Guanidine-resistant mutants are readily isolated and the mutations map to the coding region for the 2C protein. Using in vitro replication assays it has been determined previously that guanidine blocks the initiation of negative-strand synthesis. We have now examined the dynamics of RNA replication, measured by quantitative RT-PCR, within cells infected with either swine vesicular disease virus (an enterovirus) or foot-and-mouth disease virus as regulated by the presence or absence of guanidine. Following the removal of guanidine from the infected cells, RNA replication occurs after a significant lag phase. This restoration of RNA synthesis requires de novo protein synthesis. Viral RNA can be maintained for at least 72 h within cells in the absence of apparent replication but guanidine-resistant virus can become predominant. Amino acid substitutions within the 2C protein that confer guanidine resistance to swine vesicular disease virus and foot-and-mouth disease virus have been identified. Even when RNA synthesis is well established, the addition of guanidine has a major impact on the level of RNA replication. Thus, the guanidine-sensitive step in RNA synthesis is important throughout the virus life cycle in cells.

scholarly journals Internalization of Swine Vesicular Disease Virus into Cultured Cells: a Comparative Study with Foot-and-Mouth Disease Virus

2009 ◽  
Vol 83 (9) ◽  
pp. 4216-4226 ◽  
Author(s):  
Miguel A. Martín-Acebes ◽  
Mónica González-Magaldi ◽  
Angela Vázquez-Calvo ◽  
Rosario Armas-Portela ◽  
Francisco Sobrino
Keyword(s):  
Disease Virus ◽  
Cultured Cells ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coated Pits ◽  
Early Endosomes ◽  
Swine Vesicular Disease Virus ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Vesicular Disease

ABSTRACT We performed a comparative analysis of the internalization mechanisms used by three viruses causing important vesicular diseases in animals. Swine vesicular disease virus (SVDV) internalization was inhibited by treatments that affected clathrin-mediated endocytosis and required traffic through an endosomal compartment. SVDV particles were found in clathrin-coated pits by electron microscopy and colocalized with markers of early endosomes by confocal microscopy. SVDV infectivity was significantly inhibited by drugs that raised endosomal pH. When compared to foot-and-mouth disease virus (FMDV), which uses clathrin-mediated endocytosis, the early step of SVDV was dependent on the integrity of microtubules. SVDV-productive endocytosis was more sensitive to plasma membrane cholesterol extraction than that of FMDV, and differential cell signaling requirements for virus infection were also found. Vesicular stomatitis virus, a model virus internalized by clathrin-mediated endocytosis, was included as a control of drug treatments. These results suggest that different clathrin-mediated routes are responsible for the internalization of these viruses.

scholarly journals Common Host Factors Involved in the Function of the Foot-and-mouth Disease Virus and Classical Swine Fever Virus Internal Ribosomal Entry Sites

2021 ◽  
Author(s):  
Yutaro Ide ◽  
Nobumasa Ito ◽  
Takafumi Matsui ◽  
Kyoko Tsukiyama-Kohara
Keyword(s):  
Disease Virus ◽  
Classical Swine Fever Virus ◽  
Foot And Mouth Disease ◽  
Classical Swine Fever ◽  
Host Factor ◽  
Mouth Disease ◽  
Fever Virus ◽  
Host Factors ◽  
Mouth Disease Virus ◽  
Ires Element

Abstract Foot-and-mouth disease virus (FMDV) and classical swine fever virus (CSFV) both possess positive strand RNA genomes and an internal ribosomal entry site (IRES) element within their 5¢-untranslated regions. To identify common host factors involved with the activity of these IRESes, we utilized cell lines expressing a bicistronic luciferase reporter plasmid, which contained an FMDV-IRES or CSFV-IRES element between the Renilla and firefly luciferase genes. First, we treated FMDV-IRES cells with French maritime pine extract, Pycnogenol® (PYC), and evaluated its suppressive effect on FMDV-IRES activity, as anti-viral effect of PYC was reported so far. We next performed microarray analysis to identify host factors affected by PYC, and confirmed host-factor-IRES interaction by applying host factor-specific siRNAs. We found that polycystic kidney disease 1-like 3 (PKD1L3) and ubiquitin specific peptidase 31 (USP31) are involved in FMDV-IRES activity. Moreover, silencing of these factors also significantly suppressed CSFV-IRES activity. Accordingly, we suggest that PKD1L3 and USP31 are host factors that are involved in the function of the FMDV and CSFV-IRES elements.

scholarly journals Molecular Mechanisms of Immune Escape for Foot-and-Mouth Disease Virus

Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 729
Author(s):  
Bo Yang ◽  
Xiaohui Zhang ◽  
Dajun Zhang ◽  
Jing Hou ◽  
GuoWei Xu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Disease Virus ◽  
Molecular Mechanisms ◽  
Immune Escape ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Host Immune Responses ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Vesicular Disease

Foot-and-mouth disease virus (FMDV) causes a highly contagious vesicular disease in cloven-hoofed livestock that results in severe consequences for international trade, posing a great economic threat to agriculture. The FMDV infection antagonizes the host immune responses via different signaling pathways to achieve immune escape. Strategies to escape the cell immune system are key to effective infection and pathogenesis. This review is focused on summarizing the recent advances to understand how the proteins encoded by FMDV antagonize the host innate and adaptive immune responses.

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.

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