Outbreaks of the foot-and-mouth disease (FMD) have major economic impact on the global livestock industry by affecting the animal health and product safety. L-protease, a non-structural protein of FMDV, is a papain-like cysteine proteinase involved in viral protein processing as well as cleavage of host proteins for promoting the virus growth. FMDV synthesizes two forms of leader proteinase, L (Lab and Lb), where the deletion of Lab is lethal and Lb deletion is reported to be attenuated.
View Article and Find Full Text PDFJ Virol Methods
May 2024
Foot-and-mouth disease (FMD) is a contagious viral disease of cloven-footed animals. Immunization with inactivated virus vaccine is effective to control the disease. Six-monthly vaccination regimen in endemic regions has proven to be effective.
View Article and Find Full Text PDFThe relative overexpression of Coxsackie and adenoviral receptor (CAR) predisposes children to viral myocarditis. As the foot and mouth disease virus (FMDV) causes fatal myocarditis in calves, lambs, and piglets and belongs to the same family as the Coxsackie virus, we investigated the role of CAR in FMDV induced myocarditis in the suckling mice model. Swiss albino suckling mice of 5 days (n = 24) were divided into two equal groups.
View Article and Find Full Text PDFViperin, also known as radical S-adenosyl methionine domain-containing protein (RSAD2) is a multifunctional interferon-stimulated gene (ISG) that is activated during the viral infections. Viperin belongs to S-adenosyl methionine (SAM) superfamily of enzymes known to catalyze radical-mediated reactions and viperin inhibits a wide range of DNA and RNA viruses through its broad range of activity. The present study reports cloning and expression of bovine viperin in a bacterial expression system.
View Article and Find Full Text PDFThe development of a negative marker vaccine against the foot-and-mouth disease virus (FMDV) will enhance the capabilities to differentiate vaccinated from infected animals and move forward in the progressive control pathway for the control of FMD. Here, we report the development of mutant FMDV of Asia1 with partial deletion of non-structural proteins 3A and 3B and characterization of their infectivity and protection response in the guinea pig model. The deleted FMDV Asia1/IND/63/1972 mutants, pAsia and pAsia were constructed from the full-length infectious clone pAsia, the viable virus was rescued, and the genetic stability of the mutants was confirmed by 20 monolayer passages in BHK21 cells.
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