Foot-and-mouth disease pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
When FMD virus comes in contact with a host cell, it binds to a receptor site and triggers a folding-in of the cell membrane. Once the virus is inside the host cell, its protein coat dissolves. New viral RNA and components of the protein coat are then synthesized in large quantities and assembled to form new viruses. After assembly, the host cell lyses(bursts) and releases the new viruses.
Pathophysiology
Humans can be infected with foot-and-mouth disease through contact with infected animals, but this is extremely rare. Some cases were caused by laboratory accidents. Because the virus that causes FMD is sensitive to stomach acid, it cannot spread to humans via consumption of infected meat, except in the mouth before the meat is swallowed. In the UK, the last confirmed human case occurred in 1966[1][2], and only a few other cases have been recorded in countries of continental Europe, Africa, and South America. Symptoms of FMD in humans include malaise, fever, vomiting, red ulcerative lesions (surface-eroding damaged spots) of the oral tissues, and sometimes vesicular lesions (small blisters) of the skin. According to a newspaper report Foot and Mouth disease killed two children in England in 1884, suspectedly due to infected milk.[3]
There is another viral disease with similar symptoms, commonly referred to as "hand, foot and mouth disease", that occurs more frequently in humans, especially in young children; the cause, Coxsackie A virus, is different to FMDV. Both are members of the Picornaviridae family, but while FMDV belongs to the Aphthovirus genus, Coxsackie viruses belong to the Enteroviruses.
Because FMD rarely infects humans but spreads rapidly among animals, it is a much greater threat to the agriculture industry than to human health. Farmers around the world can lose huge amounts of money during a foot-and-mouth epizootic, when large numbers of animals are destroyed and revenues from milk and meat production go down.
Soon after infection, the single stranded positive RNA that constitutes the viral genome is efficiently translated using a cap-independent mechanism driven by the internal ribosome entry site element (IRES). This process occurs concomitantly with the inhibition of cellular protein synthesis, caused by the expression of viral proteases. Processing of the viral polyprotein is achieved cotranslationally by viral encoded proteases, giving rise to the different mature viral proteins. Viral RNA as well as viral proteins interact with different components of the host cell, acting as key determinants of viral pathogenesis. In depth knowledge of the molecular basis of the viral cycle is needed to control viral pathogenesis and disease spreading.[4]
References
- ↑ "Foot and Mouth Disease update: further temporary control zone established in Surrey". Defra. 2007-08-14. Retrieved 2007-08-14. Check date values in:
|date=(help) - ↑ "Foot and Mouth Disease". The Guardian. 2001-11-23. Retrieved 2007-08-14. Check date values in:
|date=(help) - ↑ "Foot and mouth 'killed people in 1800s'". The Guardian. 2001-11-23. Retrieved 2007-08-14. Check date values in:
|date=(help) - ↑ Martinez-Salas E, Saiz M, Sobrino F (2008). "Foot-and-Mouth Disease Virus". Animal Viruses: Molecular Biology. Caister Academic Press. pp. pp. 1-38. ISBN 978-1-904455-22-6.