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Ch. 18. Immune Response to Infectious Disease Viral infections Bacterial infections Protozoan Worms Ch. 19. Vaccines

Ch. 18. Immune Response to Infectious Disease Viral infections Bacterial infections Protozoan Worms Ch. 19. Vaccines. p. 447. p. 448. p. 449. p. 450. p. 451. p. 452. p. 452. p. 453. p. 453. p. 454. Response to viral infections Innate IFN-  and  by : infected cell

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Ch. 18. Immune Response to Infectious Disease Viral infections Bacterial infections Protozoan Worms Ch. 19. Vaccines

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  1. Ch. 18. Immune Response to Infectious Disease Viral infections Bacterial infections Protozoan Worms Ch. 19. Vaccines Ch. 18, 19

  2. p. 447 Ch. 18, 19

  3. p. 448 Ch. 18, 19

  4. p. 449 Ch. 18, 19

  5. p. 450 Ch. 18, 19

  6. p. 451 Ch. 18, 19

  7. p. 452 Ch. 18, 19

  8. p. 452 Ch. 18, 19

  9. p. 453 Ch. 18, 19

  10. p. 453 Ch. 18, 19

  11. Ch. 18, 19

  12. p. 454 Ch. 18, 19

  13. Response to viral infections Innate IFN- and  by : infected cell macrophages, fibroblasts, monocytes Inhibits viral replication Activates NK cells IL-12 also produced early, activates NK cells Acquired Humoral (Ab) and CMI Ch. 18, 19

  14. p. 449 Ch. 18, 19

  15. Viruses are good at evading immune response Hepatitis C can block IFN- and  activity Down-regulation of MHC Class I HSV, CMV, adenovirus Down-regulation of Class II CMV, measles, HIV Changing antigens evades humoral response Immunosuppression by infecting immune cells (e.g., EBV, HIV) Ch. 18, 19

  16. Bacterial infections Extracellular bacteria themselves toxins inflammatory response How do antibodies protect from such infections? Ch. 18, 19

  17. p. 456 Ch. 18, 19

  18. Intracellular pathogens NK cells Delayed-type hypersensitivity Bacteria also can evade the immune response Ch. 18, 19

  19. p. 457 Ch. 18, 19

  20. Sometimes immune response contributes to disease Septic shock induced by endotoxins IL-1 and TNF- Shock induced by superantigens exotoxins from Staphylococcus, e.g. Granulomas- chronic activation of CD4+ cells Lyme disease: antibodies to flagella may contribute to type III hypersensitivity Ch. 18, 19

  21. p. 459 Ch. 18, 19

  22. Protozoan diseases Protozoans often have complex life cycles Antibody effective against blood borne form CMI against intracellular stage Ch. 18, 19

  23. p. 460 Ch. 18, 19

  24. Immune response to Plasmodium infection is generally not good Complex life cycle, much of which is intracellular Trypanosomes- VSG induces a strong humoral response, but antigen constantly changes Ch. 18, 19

  25. p. 463 Ch. 18, 19

  26. Ch. 18, 19

  27. Worms Not intracellular, but not many infectious organisms Do not produce strong immune response Worldwide infection rate is very high Example: Schistosomiasis Ch. 18, 19

  28. p. 465 Ch. 18, 19

  29. Lots of IgE May not be particularly protective CD4+ cells may be more important Ch. 18, 19

  30. p. 467 Ch. 18, 19

  31. Ch. 18, 19

  32. There’s a lot to learn! What’s the best strategy? Control of infectious agent? New antimicrobials? Vaccines? Ch. 18, 19

  33. Ch.19. Vaccines Immunological principles Strategies for vaccine development Active vs passive immunization Ch. 18, 19

  34. p. 476 Ch. 18, 19

  35. p. 477 Ch. 18, 19

  36. p. 478 Ch. 18, 19

  37. p. 479 Ch. 18, 19

  38. p. 480; vs. 2004 Ch. 18, 19

  39. p. 480 Ch. 18, 19

  40. Ch. 18, 19 p. 481

  41. p. 482 Ch. 18, 19

  42. Attenuated vaccines Organisms can grow temporarily but are no longer pathogens Tend to provide a longer-lasting immune response Problems: can revert to virulence contaminants can have complications Genetic modification can reduce risks Ch. 18, 19

  43. Inactivated (killed) vaccines Must maintain immunogenicity Produce humoral response Require repeated boosters Whole vaccines can revert if not properly prepared Specific molecules can be effective and safe Ch. 18, 19

  44. Polysaccharide may be most immunogenic part of certain bacteria (Streptococcus pneumoniae) Thymus-independent antigen; not much T cell response or memory Solutions: subcutaneous injection Ab’s Hib polysaccharide is linked to carrier (tetanus toxoid) seems to activate B cell but not T cell memory Ch. 18, 19

  45. Toxoid vaccines (exotoxins) Neutralizing antibodies to toxoid Many of these are recombinant Recombinant antigen vaccines: HBsAg, produced in yeast cells Technique has been expanded Ch. 18, 19

  46. p. 486 Ch. 18, 19

  47. Ch. 18, 19

  48. These vectors could include antigens from several bacteria or viruses DNA vaccines- naked DNA is taken up by muscle cell (and dendritic cells) Long-term expression of antigen humoral and cell-mediated immunity Easier to handle than other vaccines Limitations: to protein antigens Ch. 18, 19

  49. p. 489 Ch. 18, 19

  50. Synthetic peptides B and T cell epitopes have to pick the right peptides! Some are “immunodominant”, some are suppressive Not particularly immunogenic by themselves Strategies to make multivalent vaccines which might be more effective Ch. 18, 19

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