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45 Cards in this Set

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Evasion By Hiding Types
Via Latency (2)
Via Complement Manipulation (3)
Latency- Herpes Simplex HIV
Complement- Salmonella/ Neisseria gonorrheae Streptococcus pyogenes
Evading Early Inducible Innate Defenses?
Evading Phagocytosis types? (6)
Protective Barrier
Chemotaxis Inhibition
Killing Phagocytes
Phagosome/Lysosome Fusion inhibition
Physical/Chemical Resistance to Lysosomes
Escape from Phagosome
Evading Late Inducible Innate Defenses? (5)
Misdirection of Immune Response
Host-Parasite Mimicry
Interference of Antibodies
Antigenic Variation more?
Decreased MHC Expression
Antigenic Shift v. Drift
Gene Rearrangement
Latent Herpes Simplex Virus Mechanism
Infect epithelial cells and enter into sensory neurons
S. neurons have low levels of MHC
Reactivated by stress/hormones/other infections
"cold sores"
Latency evasion-hides in woods
Latent Human Immunodeficiency
Virus Mechanism
Retrovirus puts its RNA into DNA into host's genome
T cells & Macrophages
AIDS
Latency Evasion- hides in vault in plain sight
Salmonella/E.coli Mechanism (immediate)
"O Antigens" with long chain polysccarides
Creates thick wall types?
Downsides?
Smooth v. rough strain
LPS are highly immunogenic
a lot of armor but slow can eventually take them down
Neisseria gonorrheae Mechanism
Sialic acid inhibits complement
looks like host passover chains
sialic acid at end of LPS becomes LOS- (oligo)
complement inhibition
wearing your team's colors
wolf in sheeps clothing
Streptococcus Pyogenes Mechanism
(Immediate)
M-protein expression binds to Host Factor H which destroys opsonin C3b.
turns off alarm
Staphylococcus aureus Mechanisms
(Early)
1. Coagulase/Staphlokinase
activates thrombin-fibrinogen-fibrin clot
staplokinase digest clot to initiate release
2. PVL (Panton-Valentine leukocidin) pore forming cytotoxin common in MRSA
3. Catalase inhibits respiratory burst turns H2O2 into water and O2
1. Digs a burrow in your own backyard..waits
2. Torpedoes your leukocytes
3. Disarms chemical weapons
Streptococcus pneumoniae Mechanism (early)
Polysaccharide capsule 90 different ones that make slimy wall
downside
eventually will stimulate a response due to immunogenic polysaccharides in slimy coat
Can't be eaten in one bite...can be in small ones
too much armor
Streptococcus pyogenes mech.
(early)
C5a peptidase cleaves chemoattractant C5a anaphylotoxin?
covers its tracks, throws cells off the trial
anaphylotoxins stimulate vascular permeability C5a C3a
Yersinia pestis Mechanism
(early)
YOPS YOP J (Yersinia Outer Proteins)
YOPS B/D form pores that cause cytolysis
YOP J is injected via Type III Secretion-interferes with signaling pathways, cytokine genes, and starts apoptosis
YOPS B/D rip holes in the cell
YOP J is a needle injection
Legionella pneumophilia Mech (early)
Inhibits phagosome lysosome fusion by odd coiling entry into leukocyte that throws off fusion
then they multiply and grow and lyse the cell
david copperfield escape
Mycobacterium tuberculosis Mech
(early)
Hydrophobic shield of thick waxy hydophobic cell wall of mycolic acids that cannot be penetrated by enzymes
force field
granulomas
Bacillus anthracis Mech
(early)
Poly d-glutamate unnatural isomeric polypeptide not recognized by regular peptide in phagosome
shapeshifter can't latch on
Salmonella Mech (early)
Pho-q Pho-p alarm system
resitance to cationic lysosomal anti-microbial peptides called defensins which bond to neg charge polysaccharides
Pho-q senses defensins and Mg++ drop and activates PhoP that turns on 30 genes to interfere by changing LPS turn off cytokines and decreased APC.
buddy alarm system turns off lights and goes cold. Also stops cell from warning outside.
Listeria monocytogenes Mech
(early)
Pore forming hemolysin and listeriolysin O to escape from phagosome
uses cells actin as actin based motility to move into nearby cells avoiding detection
escapes from jail then uses your own highways and ninjas around without detection JASON BOURNE
Staphylococcus aureus Mech (late)
depletion of antigen-specific T cells by superantigens

superantigen activates 20-40 percent of all CD4 cells by binding to conserved region. toxic shock.
Uses up all ammunition of host in a diversion
Streptococcus pyogenes Mech (late)
Superantigen exhaustion of antigen-specific T cells
diversion to waste ammo
Superantigen list (3)
Staphloccal Enterotoxin
Staph Toxic Shock Toxin (tSST-1)
Streptococcal Exotoxin
pathologies?
Staph food poisoning
Toxic shock syndrome
scarlet fever/shock
Mycobacterium leprae mech
(late)
Skewing Th1 Th2 balance
1. Lepromatous Leprosy switches to Th2 cytokines, thus no cell mediated response
2. Tuberculoid lyprosy has low infectivity and has Th1 cells
Lepromatous: large growth in macrophages
highly infectious
dissemeniated infection
hypergammaglobulinemiia
low t cell response
Tuberculoid opposite
local infection granuloma
calls for navy and then attacks by land
Treponema pallidum Mech (late)
Fibronectin coat (syphilis)
T. pallidum binds to host fibronectin- allows pathogen entry into host tissues and acts as a cloaking device to hide from host
Trojan horse
Staphlococcus Aureus Mech (late II)
Staphylococcal protein A (SPA) is able to bind to IgG to its Fc Region. It then loses its ability to opsonize and fix complement.
anti antibody
Neisseria meningititis Mech (late)
IgA protease because IgA is used in mucosal infection. This takes out IgA but has its fragments keep IgG from binding
takes out hosts weapons and uses them to cloak
Streptococcus pneumoniae (late)
Antigenic diversity among different pathogens keeps host from remembering the specific pathogen 90 serotypes known
keeps training and re-equiping itself
Influenza virus (late)
gene mutation/gene re-assortment
antigenic drift
antigenic shift
difference?
two identifiers?
Drift- altered hemagglutinin and neuraminidase epitope changes some inefficient memory
shift- infrequent assortment of genetic segments from another host population- very different antigens and so no resistance in population PANDEMIC
Trypanosoma brucei (late)
Gene rearrangement of variable surface glycoproteins (VSG)
like b cell rearrangment only one on the surface but process is continuous--one begins to dominate and progresses but another will wait and take over once the first is gone
waves of assault- didnt get them all
weeds

African Sleeping Sickness
Neisseria gonorrhea (late)
gene rearrangement of pilin
alters the pilus structure that allows it to attach to host epithelial cells. same as t. brucei and so host cannot get them all-need antibiotics
waves of assault- didnt get them all-need backup

gonorrhea
HIV-1 Mech (late)
Decreased expression of MHC molecules
downregulates MHC class I and beta 2 m transcription
blocks TAP transport to ER
increases MHC I turnover
Does not affect HLA-E, which if downregulated would signal NK cells to cleanse

turns off alarms quiet hostage taker
Cytomegalovirus (late)
Produces MHC class I homolog that competes for beta2m.
Binds TAP in ER and inhibits peptide translocation.
Heavy chain mimic- binds and cannot allow binding of B2m to real heavy chain. blocks peptide loading with TAP inhibition but leaves HLA-E to avoid NK.

puts in dud alarms hides
Adenovirus (late)
Retains MHC class I molecules in ER
Prevents TAP association with tapasin
List MHC expression affectors (3)
HIV-1
Cytomegalovirus (CMV)
adenovirus
HIV and CMV leave HLA-E
Multiple strategies for Streptococcus pneumoniae and streptococcus pyogenes?
S. pneumoniae has polysaccharide capsule and antigenically diverse strains (90 serotypes)
S. pyogenes inhibits chemotaxis and superantigens and has M protein
S. pneumoniae have thick wall that can be broken down eventually but has many types of walls so it takes awhile for immune system to remember
S. pyogenes covers its tracks and keeps phagocytes off its trail and causes a diversion to hyperactivate T cells to depletion and stops complement activation with M protein activating factor H
Host Regulators of Complement Activation (RCA) (5)
Factor H
C4b-binding Protein
Complement receptor type 1 (CR1)
Membrane cofactor protein (MFP)
Decay-aclerating factor (DAF)
CD59
explain??
Factor H- Cofactor that cleaves C3b by factor I; inactivates alternative pathway by dissociating C3bBbcomplex
C4bBP- Cofactor in cleavage C4b by factor I inhibiting it from C2a
CR1 MCP- Both cofactors for factor I of both C4b and C3b
DAF- binds C3 convertase of both classical and alt pathways
CD59- inhibits formation of MAC by interfering with deposition of C9 molecules
Evading Phagocytosis with protective barriers (2)
Staphylococcus aureus?
Streptococcus pneumoniae?
S. aureus coagulase/staphlyokinase
S. pneumoniae
diverse capsule
Evading by chemotaxis inhibition (1)
Streptococcus pyogenes
C5a peptidase (C5a C3a inhibition)
Evading by killing phagocytes (2)
Staphylococcus aureus
Yersinia pestis
S. aureus PVL which causes pores
Y. pestis YOPS YOP J
Evasion by stopping phagosome lysosome fusion (1)
Legionella pneumophilia
L. pneumophilia enters in a strange way that stops fusion
Evasion by misdirecting immune response (3)
Staphylococcus aureus
Streptococcus pyogenes
Mycobacterium leprae
S. aureus S. pyogenes- superantigens

M. leprae- switch to Th2 to lower cell mediated response
Host Parasite Mimicry (1)
Treponema pallidum
coats itself with fibronectin
Interference with antibody function(2)
Staphylococcus aureus
Neisseria meningititis
S. aureus has SPA (s. Protein A) that disables IgG by binding to Fc region
N. meningititis dissolves IgA and the bits of IgA continue to bind to prevent IgG.
Evasion through Antigenic variation (4)
Streptococcus pneumoniae
Influenza virus
Tripanosoma brucei
Neisseria gonorrhea
S. pneumoniae serotypes 90 in nature
influenza H#N# have antigenic shift and the worse antigenic drift
T. brucei gene rearrangement wave syndrome of VS gene
N. gonorrhea of pilin - waves of infection
Argh just what does Staphylococcus aureus do?? (5)
coagulase/staphlokinase
PVL pore forming
H2O2 inhibition
Superantigens
IgG neutralization
So it hides before phagocytosis, it torpedoes our own cells, it neutralizes our poisons it uses diversions to take out all T cells and it takes out IgG by binding to Fc region
Evasion by physical/chemical resistance to lysosomal damage (4)
mycobacterium tuberculosis
Bacillus anthracis
Salmonella
Staphlococcus aureus
M. tuberculosis hydrophobic shield of mycolic acids
B. anthracis poly D glutamate unrecognized
Salmonella PhoP Phoq system against defensins
S. aureus breaks down H202 into H2O and O2
Evasion by escape from phagosome (1)
Listeria monocytogenes
gets out of phagosome with pore forming hemolysin and phospholipase C.
It thens uses cells actin to get into another cell
JASON BOURNE PATHOGEN