Bacterial and viral vaccines Flashcards
1
Q
What are the differences between live and killed vaccines?
A
Live
- Long lived immunity
- Good immune response (like infection) - IgG, IgA
- Cell-mediated immunity
- Requires cold chain
- insufficient attenuation means that the pathogen can revert to wild type
- Immunosuppressed (risk of persistent infection)
- Foetal damage
Killed
- Short or long
- IgG (needs boosters)
- poor CMI
- Stable
- Inactivation and immunogenicity
- Contamination
- Toxicity/ allergy
- Autoimmunity
2
Q
What are vaccine adjuvants?
A
- Adjuvants can enhance the immunity against the vaccine -
usually a microbacteria component such as cell wall - In the absence of an adjuvant the immunity starts and then just fades away
- Promote uptake and Ag presentation
- Stimulate correct cytokine profiles
3
Q
Give an example of an adjuvant?
A
- Aluminium salts
- Form trapped particles, slow release of Ag, large number of macrophages exposed
4
Q
What are the outcomes of bacterial capsular polysaccharides as vaccines?
A
- poor ags
- short term memory; no T-cell immunity
- Less immunogenic in children <2yrs - poor IgG2 responses
- Enhance immunogenicity by protein conjugation with toxids D/T + outer membrane proteins - gives long term immunity in kids
5
Q
3 examples of capsular polysaccharide vaccines?
A
- MenC vaccine
- HiB vaccine
- Pneumococcal vaccine
6
Q
What is a conjugation vaccine?
A
- Conjugation links polysaccharide ag to protein carrier (e.g. diptheria/ tetanus) that the infant’s immune system already recognises in order to provoke an immune response
7
Q
How do polysaccharide antigens work?
A
- PS binds to BCR and here is poor activation
- No T-cell help
- Small amount of Ab produced - not very specific and no drive to form more
8
Q
How do conjugate vaccines work?
A
- With a conjugation, the proteins is presented to CD4+ Th cells
- Causes Th cell to produce IL-4,5,6,10
- These act on B cell and cause the production of many more, specific abs
9
Q
Why before 2014 was there no vaccine for Men B?
A
- Group B has a completely different capsule – has sialic acid on the surface (along with most other eukaryotic cells)
- Cant do a normal vaccinea s itll mount an immune response to all cells – need a different type
10
Q
How does Bexsero (MenB vaccine) work?
A
- Factor H Binding Protein (fHbp) – Pathogens can bind factor H to their surface, stopping the immune response
- Neisseria Heparin Binding Antigen (NHBA) – allows it to recognise the heparin that is expressed on pathogen surface
- Neisseria Adhesin A (NadA) – allows it to recognise the adhesin molecules
11
Q
What are some issues with Bexsero?
A
- more reactogenic;
- not all serotypes of group B covered (unlike menC)
- Some cross-protection against menW
- £75 per dose – needs to be £20 for cost effectiveness.
- 88% efficacy and strain coverage
- Duration of protection – 10 years
- 30% reduction in carriage rates
12
Q
What is the pertussis vaccine?
A
- Whole cell vaccine - killed organisms
- New low risk acellular vaccine
- adhesin + pertussis toxoids + outer membrane proteins
- Blocks adhesion and neutralises toxin - antibody
- Very effective
13
Q
Why are we having to vaccinate more and more people, and give more boosters?
A
- Heard immunity is failing due to people not getting vaccinated
14
Q
Why is it hard to make a vaccine for influenza?
A
- Lots of potential for the influenza virus to mutate
- 15 types of HA, 9 types of NA
- Segmented -vs ssRNA genome
- Segmented -> reassortment
- RNA -> no proof reading on RNA polymerase
- Antigenic drift
- Antigenic shift
15
Q
What is the trivalent flu vaccine?
A
- 70% protection for 1 year
- 2A +1B surface antigens:- inactivated, split.
- 2011- 2012
- A/California/7/2009 (H1N1)-like virus; (swine flu pandemic strain)
- A/Perth/16/2009 (H3N2)-like virus; and
- B/Brisbane/60/2008-like virus.
- Another B added, due to a widely circulating virulent strain
