MIMG 101 Lecture Notes - Lecture 26: Type Three Secretion System, Pathogenicity Island, Spi1

• School: UCLA
• Department: Microbiology, Immunology, and Molecular Genetics
• Course: MIMG 101
• Professor: G U N S A L U S& B R A D L E Y

Document Summary

Host: activate defense mechanisms, change metabolism to compete for nutrients, changes that are a result of pathogen subverting host systems, activation of cell suicide. Pathogen: activate systems to ensure infection, elude/neutralize host defenses. Obligate: restricted to intracellular survival, chlamydia, toxoplasma. Facultative: both intracellular and extracellular survival, salmonella, shigella, legionella, leishmania. Advantages of intracellular: nutrients, no competition, unchanging environment, sequestered from immune response antibodies, dissemination by migratory cells. Disadv of intracellular: need to enter, need to defend against cellular defenses lysosomes, need to exit to disseminate and transmit to other hosts. Endocytosis/phagocytosis: zippering mechanism into membrane bound vacuole, recognize and adhere, endocytosis, primary phagosome, secondary phagosome, acidification through h+/atpase pump, immature still, full lysosome, mature, more hydrolytic. Micropinocytosis: membrane ruffling receptor mediated endocytosis, active invasion salmonella induces membrane ruffling, then is taken up into host. Pathogenicity island spi1: encodes proteins for needle complex, effector proteins, virulence factors, (cid:272)auses a(cid:272)ti(cid:374) at e(cid:374)try site to disasse(cid:373)(cid:271)ly, reorga(cid:374)ize, reasse(cid:373)(cid:271)ly i(cid:374)to (cid:862)splash(cid:863)