Microimmune Lecture 20 Study Notes.docx

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Western University
Microbiology and Immunology
Microbiology and Immunology 3300B

Microimmune Lecture 20 Study Notes 1. What happens when we are infected with a pathogen? -wound healing induced, complement destruction (picked up by macrophages/DC in the tissue) -DC migrate to lymphnodes, phagocytosis, NK cells activated, cytokines and chemokines produced -pathogens phagocytosed in lymphoid tissues -adaptive immunity initiated by migrating DC -infection cleared by specific antibodies, T cell-dependent macrophage activation and cytotoxic T cells 2. What virus has coevolved successfully? -JC virus -infected 90% of all humans -initial infection is in the GI tract and largely asymptomatic (infects us at very young age; contaminated water or food) -almost everybody has it but it doesn’t harm its host; good at spreading; live long infections -pathology only in immunosuppressed patients -non dangerous environmental bacteria/virus and converts it into a human pathogen 3. What virus has not coevolved successfully? -Ebola -infection is very rare, occurred in the 1970s -highly lethal (50-100%) mortality -person-to-person transmission is rare: this is because rapid death is caused; otherwise the virus is easily spread -persistent/latent infections do not occur 4. Discuss evolution of malaria/O type etc. -malaria appeared 200mya when mammals appeared -humans and chimps diverge from the same common ancestor -human/chimp strain of malaria appeared 200mya -we developed the o blood type after splitting from chimps – 5 mya -o protects from malaria -begin to see mutations protecting us against malaria in the areas where it is endemic; as humans migrate out of Africa 80 000 ya -malaria evolving in response to these changes 5. Discuss the evolution of HIV. -women/family in the sex trade frequently exposed to HIV but never got it -they sequenced the MHC1 and MHC 11 alleles; found that MHC 11 were enriched with alleles that were protected allowing them to survive -the protective alleles were: HLA-A2 6802and HLA-DRB1*01 6. What were the first cases of HIV? -oldest HIV-1 was in 1959 -suspected species “jumped” into humas in 1931 (HIV-1) and in 1940/1945 (HIV-2 A&B) 7. What are the goals of a host pathogen? -minimize loss of fitness -select successful MHC haplotypes (get the right MHC to interact) -selecting resistance genes -“selection” of less-virulent pathogen strains -host wants to survive and reproduce; selecting for pathogens that aren’t hypovariable 8. What are the goals of a pathogen? -maximize reproductive success -host survival (at least until transmitted) -avoid immunity -modulation of virulence 9. To be a pathogen you must… -be able to survive in the human b ody (pH, temperature etc) -be able to avoid or modulate the immune response to allow your own survival -most microorganisms are not pathogens -most pathogens have immune-avoidance mechanisms 10.How does Borellia prevent opsonization? -causes lyme disease -coats itself in factor H -inhibits complement deposition -bound by exotoxin which binds factor H and turns it off -factor H only binds to self proteins to regulate it; it is bound by an exotoxin which will turn it off so that it can bind to the bacteria 11.How does Syphillis prevent opsonization? -causes treponema -coats its surface with host proteins; thereby hiding itself and antigens/cell surface from antibodies and complement -non-specific binding to charged lipids in bacterial membrane (immune system wont recognize it; only recognize self proteins) 12.How does streptococcus avoid the immune system? -has two proteins A & G which bind to IgG on the Fc receptors -this prevents opsonization, complementation and phagocytosis 13.What toxins shut down TLRs? -Brucella, UTIs effectively shut down TLRs (common in a lot of bacteria) -they contain TIR domains which bind to Myd88 -myd88 is important in the signaling cascade, by binding this it will prevent the myd88-TLR association 14.What does the virus pertussis do? -pertussis (whooping cough) creates a toxin that will chemically modify the G alpha subunit -permanently off; can’t switch to GTP -GPCRs are important to make chemokines (CXCL8) so that immune cells can get out of the blood, without this pathway they won’t make it to the site -GPCR is also important in production of superoxide (respiratory burst); so even if the immune cells make it to the site; won’t be an effective way to kill it 15.What are other ways to disrupt phagocytosis? -once the bacteria is internalized, pertussin avoids respiratory burst all together -other bacteria such as brucella or staphylococcus express superoxide dismutase which converts superoxide into hydrogen peroxide, but also expresses catalase which converts that into hydrogen and water -tuberculosis and leprosy will prevent fusion of granules/lysosomes to the phagosome -chlamydia and legionelle will alter its membrane so they appear like some other cell in the body (lipids) so nothing will fuse to it -tuberculosis and leprosy can make it to the end where their phagosome is acidified; but they can survive in this environment 16.What is killing immune cells? -streptococcus and pseudomonas contain hemolysin and leukolysins -these are pore-forming and lyse leukocytes -best way to avoid immune system is to kill it (poke hole; contents spill out) 17.What is listeria? -bacteria -doesn’t slow growth when refrigerated 18.How does listeria get into our body? -gain entry through the gut by cell extrusion -go in through vili in the gut -collect in divits; tight junctions supposed to block but the junction is being moved to where its not supposed to be so it pops out of place; bacteria has entry to the body 19.Discuss entry. -listeria has two proteins InIA and InIB -required to gain entry -get a reorganization of junctions in order to extrude an epithelial cell -results in a direct infection of the epithelia 20.What happens once it is inside? -can go to the lymphatics and has access to resident immune cells -targets macrophages 21.What happens during invasion of macrophages? -goes to the macrophage by PRRs and gets taken up by the phagosome
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