Validation of a binary ethylenimine (BEI) inactivation procedure for biosafety treatment of foot-and-mouth disease viruses (FMDV), vesicular stomatitis viruses (VSV), and swine vesicular disease virus (SVDV)

2021 ◽  
Vol 252 ◽  
pp. 108928
Author(s):  
Ping Wu ◽  
Yelitza Y. Rodríguez ◽  
Benjamin J. Hershey ◽  
Yadata Tadassa ◽  
Kimberly A. Dodd ◽  
...  
1974 ◽  
Vol 72 (1) ◽  
pp. 61-65 ◽  
Author(s):  
R. F. Sellers ◽  
K. A. J. Herniman

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.


2008 ◽  
Vol 89 (2) ◽  
pp. 485-493 ◽  
Author(s):  
Graham J. Belsham ◽  
Preben Normann

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.


2009 ◽  
Vol 83 (9) ◽  
pp. 4216-4226 ◽  
Author(s):  
Miguel A. Martín-Acebes ◽  
Mónica González-Magaldi ◽  
Angela Vázquez-Calvo ◽  
Rosario Armas-Portela ◽  
Francisco Sobrino

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.


2018 ◽  
Vol 62 (4) ◽  
pp. 431-437
Author(s):  
Ya-Li Liu ◽  
Yao-Zhong Ding ◽  
Jun-Fei Dai ◽  
Bing Ma ◽  
Ji-Jun He ◽  
...  

Abstract Introduction: The extremely high genetic variation and the continuously emerging variants of foot-and-mouth disease virus (FMDV) of Southern African Territory (SAT) serotypes including SAT1, SAT2, and SAT3 make it necessary to develop a new RT-PCR for general use for monitoring viruses based on the updated genome information. Material and Methods: A FMDV SAT-D8 one-step RT-PCR was established based on the 1D2A2B genes of the SAT serotype viruses with a multiplex primer set. FMDV A, O, C, and Asia 1 serotypes, other vesicular disease viruses, inactivated SAT viruses, and 125 bovine, ovine, caprine and porcine tissue samples collected from the Chinese mainland were included for evaluating the assay. Results: The new RT-PCR was proven to be specific without cross-reactions with Eurasian FMDV, swine vesicular disease virus (SVDV), Seneca valley virus (SVV), or other common viral pathogens of cattle, sheep, goat, and pig. An around 257 bp-sized amplicon clearly appeared when the inactivated SAT viruses were detected. However, all 125 samples collected from FMDV-susceptible animals from the Chinese mainland which has not known SAT epidemics showed negative results. Conclusions: A FMDV SAT-D8 one-step RT-PCR is a promising method for primary screening for FMDV SAT serotypes.


Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 729
Author(s):  
Bo Yang ◽  
Xiaohui Zhang ◽  
Dajun Zhang ◽  
Jing Hou ◽  
GuoWei Xu ◽  
...  

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.


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