Microbial immune evasion mechanisms Flashcards
1
Q
How do capsules help evasion?
A
- Block opsonisation and phagocytosis - poor recognition for antibodies
- Bind factor H on the surface to inhibit complement
- Serum resistance
2
Q
What are luekocidins?
A
- Toxins that damage the membranes of T cells and neutrophils
3
Q
How does pertussis adhere to ciliated cells?
A
- Ciliastatic - stops the cilia action
4
Q
How does mimicry help evade immune system?
A
- Some pathogens have very similar proteins on them to host cells, stopping the response against them
- eg Streptococci have M proteins, which are very similar to cardiac muscle valve proteins (can cause rheumatic fever if immune response mounted)
5
Q
How are some pathogens protected against complement?
A
- LPS and CApsules
- Factor H and capsule stop binding
C5a proteases, stopping chemoattractant signals
6
Q
What happens to pathogens that get inside the cell?
A
- Some stay in endosome after phagocytosis, inhibiting P-L fusion, blocking acidification (mycobacteria)
- Some can resist the digestion and ROIs in PLs - catalase
- Some release peptides into the MHC, creating antigens to recruit the wrong type of immune response - stops CTLs and phagocyte activation
- Some produce Fc receptors, causing abs to bind the wrong way around
- Some can escape into the cytoplasm (listeria)
7
Q
How do we kill pathogens that get into the cytoplasm or vacuoles?
A
Cytoplasm = CD8 CTLs, NKs
Vacuoles = CD4 Th1 -> mp killing
8
Q
How do pathogens evade the adaptive immunity?
A
- Concealment of ag - hide inside cells, privileged sites, block MHC antigen presentation (herpes -ve TAP protein), surface uptake of host molecules (CMV and b2microglobulin)
- Immunosuppresion - decrease MHC, receptors, induce or inhibit apoptosis, Th1-2 switch or IgA proteases
- Antigenic variation
- persistence/latency / reactivation
9
Q
What does streptococcus pneumoniae do to evade mechanisms?
A
- Infected through aerosol mechanisms
- Adheres to nasopharynx and colonises - produces sIgA proteases to protect in the airways
- If they start to invade locally, they can get inhaled to the lungs and bypass defences
- Escapes phagocytosis because of capsule
- Makes pro-inflammatory response through teichoic acd (similar to LPS/ endotoxin)
- Also damages endothelial cells through pneumolysin -> pneumonia
10
Q
Viruses and evasion
A
- Latency - VZV, HSV
- Decreased antigen presenting by binding to TAP and inhibiting peptide transfer to MHC (HSV)
- Decreased MHC expression (CMV)
- Mutation of epitopes
11
Q
What is phase variation?
A
- Switch genes n and off to stop and start expression of antigen
12
Q
Why has influenza got such a potential for variation?
A
- 15 different HA and 9 different NA
- Has a segmented genome so can undergo recombination
- Has an RNA genome so makes lots of mistakes during replication
- Antigenic drift - mutation and selection
- Antigenic shift - gene reassortment
