Foot and Mouth disease Virus Group 2.pptx

Foot and Mouth Disease Virua

1.   FOOT AND MOUTH DISEASE VIRUS 1

2. INTRODUCTION: Foot and mouth disease is caused by a highly contagious “ Picornavirus “ called Foot and Mouth disease virus. These are small non-enveloped RNA viruses, because they contain no lipids so they are ether resistant. They cause a highly contagious disease in cloven hoofed animals like cattle, sheep, deer and goats. FMDV replicate in the cytoplasm . CLASSIFICATION OF VIRUS : Order: Picornavirales Family: picornaviridae Genus: Aphthovirus Discovery: The cause of FMD was first shown to be viral in 1897 by Friedrich Loeffler he passed the blood of an infected animal through a chamber land filter and found that the collected fluid could still cause the disease in healthy animal. 2

3. STRUCTURE OF fmdv CAPSID It is non-enveloped with icosahedral symmetry and has a diameter 30nm . Capsid has 60 copies viral proteins, VP0, VP1 and VP3 , organized in the form of 12 pentamers . The final maturation cleavage of VP0 occurs in the presence of RNA, to produce VP4 (the N-terminal 85 residues of VP0) and VP2. The viral proteins are VP1-4 (numbered from the largest to the smallest). VP1, VP2 and VP3 are present on the outer side of the shell, while the N termini of VP1-3 and all the 60 VP4 molecules are completely internal . 3

4. Capsid are extremely sensitive to low-pH and elevated temperature . Capsid release their genome into the host cell from an acidic compartment, such as endosome, and in the process dissociate into pentamers . Pentamer is a protein made of 5 proteic sub-units composing polyhedral capsid. 4

5. GENOME: Genome is linear strand of positive sense ssRNA Genomic size is 7.5-8.5 kb . Covalently linked to the 5’ end of the RNA is a small protein known as VPg (virus protein genome linked). The covalent link is via the –OH group of a tyrosine residue at position 3 of the VPg . The 3’ end of the RNA is polyadenylated . 5

6. The genome consists of one very large ORF having untranslated regions. Within the untranslated regions there is much secondary structure . The long UTR at the 5’ end contains an internal ribosomal entry site (IRES) type 2. The genome mainly consists of three regions. The P1 region encodes the structural polypeptides. The regions P2 and P3 encode the non-structural proteins associated with replication. The shorter 3’ UTR is important in negative sense (-) synthesis. 6

7. REPLICATION OF FMDV Attachment Life cycle occurs in cytoplasm of the host cell.   Integrin Protein :membrane receptor that functions as cell adhesion molecules and respond to extra cellular matrix It bind to arginine-glycine-aspartic acid (RGD) -dependent integrin including αvβ3 and αvβ6 . Heparin Sulphate : it is a glycosaminoglycan (GAG) most abundant hetero polysacchride on the body. The attachment sites of FMDV are on in the VP1 protein of capsid. 7

8. Penetration Virus can enter the cell by endocytosis. Genome uncoating occur in cytoplasm. Once virus genome is free , VPg is removed from 5’ end by a cell enzyme. Translation And Replication The RNA of the virion acts as mRNA. 5’ cap of mRNA is absent but possesses an internal ribosomal entry site (IRES) element within the 5′ untranslated region (5′UTR) . Virus proteins are synthesized by IRES-mediated translation  8

9. Translation start by internal entry of the 40S ribosome within the IRES, facilitated by cellular factors IRES trans-acting factors (ITAFs) .   IRESs do not bind the 40S subunit directly, but through the  EUKARYOTIC INITIAION FACTOR eIF4G-BINDING SITE. Replication through a ds RNA intermediate that is formed using viral RDRP From negative strand RF, new plus-strand synthesis begin. mRNA is translated into a poly protein , then cleaved to eleven individual proteins. 9

10. Assembly and Exit FMDV undergoes self- assembly The cleavage products of the P1 region are assembled, containing VP0, VP1, and VP3 proteins, into monomer. Five monomers assemble into the pentameric capsid subunit. 12 pentamers join to form a procapsid The maturation cleavage reaction (VP0 to VP2 and VP4) takes place. Lysis of cell releases the virion .   10

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12. TRANSMISSION OF FOOT AND MOUTH DISEASE VIRUS Direct contact with infected animal. Aerosol droplets from infected animals. Contact with contaminated fomites. Spread long distance via wind currents . Via milk, semen, saliva, feces , urine, breath. Susceptible animals are: Cattle, sheep, pigs and goats. ROUTES OF SPREAD Inhalation ( lungs) Ingestion (gut) Sexual transmission Conjuctival membrane (eyes) Damaged skin 12

13. DIAGNOSIS OF FMDV Diagnosed by testing of samples of Blood samples Vesicular fluids ,epithelial tissue . 13

14. SIGNS AND SYMPTOMS OF FMDV Clinical signs: Cattle Oral vesicles Tongue, dental pad, soft palate, nostrils Excess salivation, nasal discharge Teat lesions Decreased milk production Foot lesions Inter digital space Coronary band Clinical signs: Pigs Hoof lesions Coronary band, heel, inter digital pace Vesicles on snout Sudden death in young Symptoms in sheep and goats : Agalactia in milking sheep and goats 14

15. PREVENTION OF FMDV Highly infectious but prevented by biosafety measures. Clean yourself and everything you carry. Do inspect animals regularly Separation of sick animals Vaccination at an interval of 6 months Report any signs of disease to Vet. Wash hands after contact with livestock. Control of FMDV Disinfect equipments and floors with household bleach. Remove all organic matter (manure, dirt, feed etc.) 15

16. TREATMENT OF FMDV No specific treatment Treated to prevent Secondary infection. LOCALIZED TREATMENT Rinse the ulcerated vesicles by Normal saline , 1% citric acid , 1% Potassium permaganate Juices of sour fruits for washing ulceration in mouth, tongue . Bandage all legs for prevention of flies. After cleaning the wound with normal saline and drying apply antiseptic, then ointment .   GENERALIZED TREATMENT In generalized treatment use Biocevit or Bio- ADE +B complex to enhance the immune system. For prevention of secondary infections use Bio – Tylosin . Or Bio -D. O. C antibiotic.     16

17. 17 Department for Environment Food and Rural Affairs. "Foot and mouth." DEFRA, UK. 2011. The Center for Food Security & Public Health. "Foot and Mouth Disease." Iowa State University College of Veterinary Medicine. 2007. Grubman MJ, Baxt B. Foot-and-mouth disease.  Clin Microbiol Rev. 2004;17:465–493. doi : 10.1128/CMR.17.2.465-493.2004. Orsel K, Dekker A, Bouma A, Stegeman JA, de Jong MC. Quantification of foot and mouth disease virus excretion and transmission within groups of lambs with and without vaccination. Vaccine (2007) 25(14):2673–9.10.1016/j.vaccine.2006.11.048 Alexandersen S, Mowat N. Foot-and-mouth disease: host range and pathogenesis.  Curr Top Microbiol Immunol  (2005) 288:9–42. Yang PC, Chu RM, Chung WB, Sung HT. Epidemiological characteristics and financial costs of the 1997 foot-and-mouth disease epidemic in Taiwan. Vet Rec  JF Schijven , GBJ Rijs - 2004 - rivm.openrepository.com J Parker - Veterinary Record, 1971 - veterinaryrecord.bmj.com Moutou , F., Dufour , B. and Ivanov, Y., 2001. A qualitative assessment of the risk of introducing foot and mouth disease into Russia and Europe from Georgia, Armenia and Azerbaijan.  Revue Scientifique et Technique-Office International des Épizooties ,  20 (3), pp.723-727. Salguero , F.J., Sánchez-Martín, M.A., Díaz -San Segundo, F., de Avila, A. and Sevilla , N., 2005. Foot-and-mouth disease virus (FMDV) causes an acute disease that can be lethal for adult laboratory mice.  Virology ,  332 (1), pp.384-396. REFERENCES