Term
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Definition
• Evasion via latency
o prior to complete clearance by immune system, virus enters sensory neurons
o neurons - long lived, express little MHC
o thus, neurons containing virus are overlooked by immune system; don't activate CTLs - virus enters latent state
o reactivation occurs by the likes of stress-induced hormonal changes or other infections
o cold sores |
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Term
| HIV-1 ------------------2 |
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Definition
• Evasion via latency
o hides in mostly T lymphocytes and macrophages
o retrovirus (uses reverse transcriptase to copy and add its RNA genome to host cell's)
• Decrease Expression of MHC molecules
o Mechanism
• down-regulates MHC class I and beta2m transcription
• blocks TAP transport of peptides into the ER
• Increases MHC class I turnover via endocytosis (allele-specific)
o Notes - Effects on MHV class I appear to have specificity for certain class I molecules; that is, significant down-regulation of HLA-A and HLA-B is observed, but there is little impact on the expression of HLA-C and HLA-E. Since HLA-E is involved in NK cell inactivation, this selectivity allows HIV-1-infected cells to escape lysis by NK cells. |
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Term
| influenza virus -----------------------2 |
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Definition
• Antigen Variation – Antigenic Drift
o RNA virus w/ complex genome (prone to mistakes resulting in generation of point mutations)
o Mutations often in genes that code for HEMAGGLUTININ and NEURAMINIDASE proteins
o small changes to the genome = small changes in protein epitopes
o slight epitope changes = diminished ability for previous antibody to recognize the virus
• Antigen Variation – Antigenic Shift
o shifts are due to INFREQUENT REASSORTMENTS OF GENOMIC SEGMENTS
o usually from different host populations such as humans, pigs and birds, etc
o MAJOR DIFFERENCES in antigen expression rapidly occur - could result in PANDEMIC |
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Term
| salmonella ---------------------------2 |
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Definition
• Avoids complement pathway
o long-chain polysaccharides on "smooth" strains
o differ from "rough strains" that have short chained polysaccharides
o also known to evoke strong immunogenic responses
o these "O-Antigens" avoid complement binding
• Resists physical/chemical damage from lysosome
o must avoid digestion by cationic lysosomal anti-microbial peptides (such as defensins) - these attack the negatively charged phosphoryl groups of lipopolysaccharide (LPS)
o possesses a genetic sensing system known as the PhoP-PhoQ Regulon
o PhoQ senses presence of cationic anti-microbial peptide OR a drop in Mg++ ions (happens when lysosome-phagosome fusion occurs); it then is autophosphorylated and activates PhoP
o PhoP - transcription factor that after being activated by PhoQ, it activates multiple genes (at least 30) who products interfere with various destructive processes in phagocytes (such as structural change in LPS, reduced cytokine responses, and decreased antigen presentation. |
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Term
| neisseria gonorrheae--------------------2 |
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Definition
• Avoids complement pathway
o sialic acid in lipopolysaccharide of this pathogen (LOS - sialic acid terminal sugar in LPS - grabs factor H)
o sialic acid is an inhibitor of complement (grabs factor H)
o sialic acid is the terminal sugar of its LPS - collectively called LOS (lipooligosaccharide)
• Phase/Antigenic Variation – Gene rearrangment
o it is bacterial agent of (blank)
o expresses a PILUS STRUCTURE (allows pathogen to bind to host epithelial cells)
o numerous variations of this protein, called PILIN, that compose the pilus structure
o like trypanosome's VSGs, its pilin variations are "switched" in and out
o once immune system targets one variation (lets say, pilin A), then GENE REARRANGEMENT takes place and the pathogen begins to express a different variation of pilin (lets say, pilin B) |
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Term
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Definition
• Interfere with antibody function
o contains IgA protease (IgA - mucosal antibody)
o causes disease in which, pathogen associates with mucosal boundaries thus stimulating mostly the secretion of IgA
o IgA protease present in - breaks down IgA and uses its fragments to also defend against IgG |
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Term
| streptococcus pyogenes ----------------3 |
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Definition
• Avoids complement pathway
o M-protein expressed (virulence factor that binds factor H)
o expresses M-protein
o M-protein binds to factor H
o C3b is cleaved; complement activation avoided
• Inhibits phagocyte chemotaxis
o t produces C5a peptidase that inhibits phagocyte chemotaxis (following of phagocyte)
o C5a peptidase - cleaves the potent leukocyte chemoattractant C5a (side product of complement activation)
o C5a (together with C3a) are ANAPHYLOTOXINS (increase vascular permeability - easy diapedisis)
• Use of superantigens
o superantigens activate a large # of pro-inflammatory T-cells (TH1 and TH17)
o responses are polyclonal and involve as many as 20-40% of all CD4+ T cells - so many can lead to toxic shock syndrome
o T cell arm of immune system = state of paralysis |
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Term
| staphylococcus aureus --------------------5 |
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Definition
• Evades phagocytosis with protective barrier
o coagulase/Staphylokinase produced by (blank) which has a wall of fibrin made with help from COAGULASE - promotes clot formation and STAPHYLOKINASE - digests clot)
o Coagulase/Staphylokinase production
o Coagulase - generates a fibrin clot around cell (prothrombin --> thrombin)
o Staphylokinase - digests fibrin clot when pathogen is ready to spread
• Evasion by killing phagocytes
o Produces Panton-Valentine leukocidin (PVL)
o t is a pore-forming cytotoxin produced by some strains of this pathogen
o present in the majority of community-associated methicillin-resistant S. aureus (CA-MRSA)
• Resists physical/chemical damage from lysosome
o it has CATALASE - enzyme that breaks down H2O2 (hydrogen peroxide)
o H2O2 is essential in oxidative respiratory burst
• Use of superantigens
o superantigens activate a large # of pro-inflammatory T-cells (TH1 and TH17)
o responses are polyclonal and involve as many as 20-40% of all CD4+ T cells - so many can lead to toxic shock syndrome
o T cell arm of immune system = state of paralysis
• Interfere with antibody function
o neutralizes opsonizing antibodies with Staphylococcal Protein A
o it has staphylococcal protein A - binds IgG through its Fc region; after binding, IgG loses its complement fixing and opsonizing abilities. |
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Term
| streptococcus pneumoniae --------------------2 |
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Definition
• Evades phagocytosis with protective barrier
o Polysaccharide capsule expressed by this pathogen (90 diff polysaccs on cell surface create thick slimy wall - CAPSULE)
o has 90 different polysaccharides on its surface that collectively form a slimy wall – CAPSULE
o many of these polysaccharides are immunogenic, however
• Antigenic Variation
o each strain carries slightly different polysaccharide antigens in capsules
o immunity to one strain leaves individual unprotected to other strains of other "SEROTYPES" (over 90 serotypes!) |
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Term
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Definition
• Evades by killing phagocytes
o YOPs
o Yersinia Outer Proteins
o bacteria is agent of plaque
o YOP B/D - forms pores in the cell membranes of host macrophages and have been linked to cytolysis
o YOP J - injected into cytoplasm of host cells via type III secretion and interfere with signaling pathways required for various phagocytic activities, activation of cytokine genes, and can also trigger apoptosis |
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Term
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Definition
• Inhibits phagosome/lysosome fusion o causes atypical pneumonia referred to legionellosis (Legionnaire's diseases) o readily enters and grows within human alveolar macrophages
o it inhibits lysosome-phagosome fusion by entering the host cell by a specialized phagocytic process involving coiling of a single pseudopod around the bacterium
o incomplete signaling results in modification of the membranes of the phagosomes that inhibits their fusion with lysosomal granules |
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Term
| mycobacterium tuberculosis |
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Definition
• Resists physical/chemical damage from lysosome
o Hydrophobic shield
o cause of tuberculosis, lives inside macrophages o thick waxy hydrophobic cell wall components, MYCOLIC ACIDS, are not easily attacked by lysosomal enzymes or penetrated by reactive oxygen products
o surface lipids with long and short-chain fatty acids - trehalose dimycolic acid (cord factor) |
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Term
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Definition
• Resists physical/chemical damage from lysosome
o it resists killing and digestion by means of its POLY D-GLUTAMATE capsule
o someric D-configuration is not recognized by conventional proteases of lysosomes |
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Term
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Definition
• Escape phagosome (leave phagosome then live in cytoplasm)
o this pathogen relies on several molecular species for early LYSIS of PHAGOSOME
• 1. Pore-forming Hemolysin (listeriolysin O)
• 2. Two forms of phopholipase C
o ACTIN-BASED MOTILITY in cytoplasm - this pathogen interacts with host cell's actin cytoskeletal system, turning it into its own form of transportation
o this pathogen induces its own movement through the host's cytoplasm using cell actin polymerization and formation of microfilaments (cell-to-cell transmission)
o this method of spreading btwn cells protects pathogen from antibodies and other extracellular antimicrobial substances |
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Term
mycobacterium leprae
lepromatous leprosy
tuberculoid leprosy |
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Definition
• Skew the TH1 vs. TH2 balance
(BLANK) LEPROSY
o ABSENCE of cell-mediated immunity (low/absent T-cell responsiveness = no response to this pathogen's antigens) - this disease is called (blank) leprosy
o also, no TH1 cells (inflammatory helper cells); thus, no IL-2, IFN-gama, and TNF-beta; do have TH2 cell presence
(BLANK) LEPROSY
o (blank) leprosy (less harmful) - patients demonstrate cell-mediated immunity (inflammation cytokines) but little TH2 cells
o also, no TH2 (antibody formation helpers) cell activity/presence, thus, no IL-4, IL-5, and IL-10 |
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Term
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Definition
• Host-parasite mimicry – coat with host’s fibronectin
o evasion mechanism is to coat a pathogen with host products so that the immune system recognizes it as "self"
o agent of syphilis; binds host FIBRONECTIN, serves 2 purposes
• 1. bridges pathogen to host tissues
• 2. cloaks pathogen (makes invisible to immune system) |
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Term
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Definition
• Phase/Antigenic Variation – Gene Rearrangment
o African sleeping sickness
o VARIABLE SURFACE GLYCOPROTEINS - only one VSG protein can be expressed at one time
o can rearrange VSG genes through GENE CONVERSION (gene in expression site removed and replaced by another VSG gene of similar, but not identical sequence)
o host goes through waves of trypanosome VSG variants |
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Term
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Definition
• Decrease Expression of MHC molecules
o Mechanism
• produces MHC class I homolog that competes for beta2m
• binds TAP in ER and inhibits peptide translocation
o Notes
• this virus encodes an MHC class I heavy chain homolog; this heavy chain mimic can bind beta2m, thus preventing the association with the real heavy chain necessary for transport to the surface.
Displaced MHC heavy chains are "ejected" into the cytoplasm where they are fed to proteosomes for degradation.
• This virus' heavy chain mimic also inhibits TAP, thereby blocking peptide loading of HLA-A, -B, and -C molecules, but not HLA-E; this preservation of HLA-E ensures protection against NK cells |
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Term
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Definition
• Decrease Expression of MHC molecules
o it retains MHC molecules in the ER
o prevents TAP association with tapasin |
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