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MYXOVIRUSES

MYXOVIRUSES. -Dr SATHYA ANANDAM. Myxo = affinity to mucin. Myxoviruses. Paramyxo viruses. Orthomyxo viruses. Smaller Segmented RNA genome Liable to Agic variation. Larger Single piece of RNA Not liable to Agic variation. - Parainfluenza Mumps virus Measles virus

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MYXOVIRUSES

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  1. MYXOVIRUSES -Dr SATHYA ANANDAM

  2. Myxo = affinity to mucin Myxoviruses Paramyxo viruses Orthomyxo viruses • Smaller • Segmented RNA genome • Liable to Agic variation • Larger • Single piece of RNA • Not liable to Agic variation • - Parainfluenza • Mumps virus • Measles virus • Respiratory syncytial virus • Newcastle disease virus Influenza viruses

  3. Influenza Viruses • Replicate in mucus membranes • Target tissue: upper & lower respiratory tract • Cause influenza: acute respiratory disease that may occur in epidemics or even pandemics

  4. INFLUENZA • Types of Influenza : Influenza Type A Influenza Type B Influenza Type C • Host range: • Human beings. • Animals, birds, Mice. • Horses, Whales, seals, swine.

  5. INFLUENZA VIRUS Spherical virus 80 -120 microns Pleomorphism. Surface peplomers.

  6. Protein envelope INFLUENZA VIRUS

  7. Structure • -ve sense ssRNA viruses with segmented genome(8 pieces) • RNA segments + nucleoprotein form a nucleocapsid • RNA dependent RNA polymerase essential for transcription

  8. Antigenic structure : 1. Internal antigen: Three serotypes: A,B &C. These proteins don’t cross react Ribonucleoprotein. M protein 2. Envelop antigens Lipid layer : It consists of two surface peplomers a. Haemagglutinin:Triangular shaped and numerous Glycoprotein. Haemadsorption & Haemagglutination. b. Neuraminidase: Mushroom shaped peplomer. Glycoprotein enzyme. Strain specific.

  9. Haemagglutinin • Binds to host cell surface receptor(RBC & Respepi cells) • The target of neutralizing Abs • Haemagglutinates RBCs from various animal species • H1 -15 Neuraminidase • Cleaves neuraminic acid to release virus progeny from infected cells • Degrades the protective layer of mucin in the respiratory tract • Plays a min role in immunity to influenza • N1-9

  10. Neuraminidase Cleaves neuraminic acid to release virus progeny from infected cells Haemagglutinin Binds to host cell surface receptor

  11. Haemagglutination • Fowl erythrocytes & virus adsorbs on mucoprotein receptors to produce hemagglutination. • Takes place from 00 C to 370C • Generally Type A & Type B strains. • Haemagglutination titer Highest dilution of viral suspension causing agglutination of fixed quantity of RBCs. • Useful for titration & detection of virus from culture fluids. • Standardisation of killed influenza vaccines.

  12. Types of Influenza virus I- Type A virus: • Infects humans as well as animals • Undergoes continuous Antigenic variations • Many animal species have their own influenza A virus • Pigs & birds are important animal reservoirs playing a role in occurrence of influenza epidemics

  13. II- Type B virus: • causes milder disease • Infects human only • Undergoes Antigenic variation but only Agic shift III- Type C virus: • Of doubtful pathogenicity • Antigenically stable

  14. Antigenic VariationAntigenic Drift • Gradual sequential change in antigenic structure occurring regularly at frequent intervals • It is spontaneous point mutation of known strains of influenza causing minor change of an amino acid sequence of HA or NA. • Occurs in influenza A & B • Periodic epidemics of influenza

  15. Antigenic VariationAntigenic Shift • It is the process in which the genetic segment encoding for envelope glycoproteins (HA&NA) is replaced by another one from a different strain through genetic reassortment causing replacement of the original HA or NA by a new one

  16. Antigenic shift • Due to reassortment. • Abrupt, drastic, discontinuous variation in antigenic structure  completely new strain. • In the case of influenza A it occurs periodically. • Apparently "new" HA and / or NA are found in the circulating viral strains. • There is little immunity for this new one. • Results in epidemic / pandemic.

  17. This is responsible for appearance of completely new strains to which no one is immune & not covered by annual vaccinations Chicken H5N1 Human H3N2 H5N2 influenza A

  18. CULTURE: Rhesus monkey kidney cell cultures. Continuous cell lines. Growth: Cytopathic effects are not prominent. Demonstrated by Haemagglutination titer in culture fluid. Serial passage of virus in embryonated egg: Strain shows high haemagglutination titers with low infectivity : Von Magnus phenomenon

  19. Monkey kidney cell culture Uninfected Monkey kidney cell culture infected

  20. Mode of transmission • Highly contagious disease with person to person transmission • Three modes of transmission Droplet Air- Borne Contact Direct Indirect

  21. Pathogenesis Viral NA degrades the protective mucin layer Allowing the virus to enter the cells Replication inside the cells Cilia damage Epithelial desquamation Epithelial cells of respiratory tract The infection is limited to the respiratory tract….why? There are proteases there essential for HA to be active Despite systemic symptoms, no viremia….why? Those symptoms are due to cytokines

  22. Clinical pictureIncubation period: 1-4 days FEVER Sore throat • . cough Complications headache • pneumonia and respiratory failure • Reye,s Syndrome diarrhea vomiting 50% of infected people don’t present any symptoms But still contagious This makes it difficult to stop the spread of the disease

  23. Reye’s Syndrome • Acute encephalopathy with hepatic necrosis and renal involvement in children & adolescents (2-16 yrs) • A rare complication of influenza A, B and Varicella- Zoster infection • There is an association between salicylate intake and subsequent development of Reye’s Syndrome

  24. Laboratory Diagnosis • Specimen: nasal washings, gargles, throat swabs 1- Direct Virus Demonstration: • Direct Immunofluorescence: for rapid Ag detection in nasal aspirates, not very sensitive • RT-PCR: for detection of viral RNA

  25. 2- Viral Isolation: specimens are inoculated into embryonatedeggs or primary monkey tissue culture • Cell culture are tested for the virus by Haemagglutination

  26. Serology : • Antibody demonstration. • Complement fixation test. • Haemagglutination inhibition test. • (Strain currently causing infection). • Radial immunodiffusion on agarosegel screening test. • 4. PCR: Detection of viral RNA

  27. EPIDEMIOLOGY • Sporadic outbreaks ( Epidemics ) :Type B • Type C : Mild and unapparent infections. • Pandemics: Type - A • World - wide • Winter months ( October to December ) • Pre - school children. • Elderly people with high mortality.

  28. Migratory water birds Domestic birds How Novel strain transmission ( First Mechanism ) Pandemic strain

  29. Migratory water birds Domestic birds How Novel strain transmission ( Second Mechanism ) Pandemic strain

  30. Influenza Pandemics 2004-06 1918: “Spanish Flu” 1957: “Asian Flu” 1968: “Hong Kong Flu” 128deaths out of 225cases Vietnam, China, Cambodia, Dijiboti, Egypt, Indonesia Thailand , Iraq, Azerbajjan&Turkey till 6 june 2006 50 million deaths 1-4 million deaths 1-4 million deaths A (H1 N1) A (H2 N2) A (H3 N2) A(H5N1)

  31. Prophylaxis I-vaccines • Inactivated • Live attenuated • Amantadine& Rimantadine • Zanamavir & Oseltamivir II- chemoprophylaxis

  32. I- Influenza vaccines • A new vaccine is formulated annually using the types & strains of influenza predicted to be the major problem for that year. • Predictions are based on world wide monitoring of influenza • The vaccine is multivalent

  33. 1) Inactivated vaccine: • Whole killed vaccine prepared in chick embryo • Recommended for persons at increased risk for influenza related complications & their contacts • Given by intramuscular injection • It has a short lived protective effect so usually given in the fall, for the protection to be high in December & January • Given every year as protection is short lived, and also as the most effective strains for the vaccine will change due to shift or drift

  34. 2) Live attenuated(cold adapted) • Recently approved only for healthy individuals • Prepared from temperature- sensitive mutants that can replicate in cooler nasal passages (33C) but not in warm lower respiratory tract • Given by nasal spray thus could provide mucosal, humoral & cell-mediated immunity

  35. GENERAL PROPHYLAXIS: Isolation of case. Identifying the source and removal . Safe supply of Drinking Water. Proper hand washing procedures.

  36. II- Chemoprophylaxis 1)Amantadine & Rimantadine: • Prevent penetration & uncoating of the virus by blocking M2 protein • Treat & prevent influenza A only • Given to high risk groups • Resistance develops rapidly

  37. 2) Zanamavir & Oseltamivir (tamiflu) • They are neuraminidase inhibitors, inhibiting the release of virus from infected cells • This limits the infection by reducing the spread of virus from one cell to another • For treatment not prevention • Effective against influenza A &B

  38. Control of transmission

  39. PICTORIAL PRESENTATION of SOME PROTECTORS GOGGLES N-95 MASK OR GOWN (MUST FOR LAB WORK TRIPLE LAYER MASK SHOECOVERS GLOVES

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