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Stage 2 > Immunology Theme 3 > Flashcards

Immunology Theme 3 Flashcards

1
Q

why is there a lag phase after a virus is administered, outline what occurs after this

A

Lag phase because antigen needs to be taken up presented to T cells, which then initiate B cells.
B cells make antibodies immediately, but also make memory cells

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2
Q

what are the primary and secondary antibodies produced

A
  • Primary – IgM antibodies

* Secondary – switch to IgG dominated response

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3
Q

outline the characteristics of memory b-cells and where do they develop

A

develop in lymph nodes

  • Long-lived (quiescent  alive but inactive), high affinity, class switched antibody
  • Affinity maturation – antibody will be more complementary to the antigen/ evolved better to bind to it
  • Undergo Somatic hypermutation  allows antibody genes to produce a higher quality antibody- undergoes genetic rearrangement
  • Recombination  allows antibody to switch classes depending on the need
  • Circulate and are more easily activated than naïve B-cells
  • Memory T-cells also produced
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4
Q

outline the involvement of b-cell in the secondary immune response

A

• Secondary immune response is quicker, stronger and an IgG response predominates

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5
Q

what infections are IgG and IgA responses better for

A

IgG- tissue infection

IgA- mucosal infection

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6
Q

what occurred in the case of the small pox vaccine

A

after the vaccination antibody levels had no significant decline here where as T-cell memory declined

  • Immunity is long-lasting
  • Memory is maintained in the absence of antigen e.g. small pox
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7
Q

outline Variolation for smallpox

A
  • Smallpox has a long history of pestilence
  • Widely used in the 18th century
  • Inoculation of live virus from pustules people with less severe symptoms of the disease, scratch the skin of someone who hadn’t got it- this provided some protection but killed those who were inoculated
  • Mild disease and protective immunity
  • Effective but killed 3%
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8
Q

outline how Vaccination against cowpox provides immunity against smallpox. mention why this may only be the case in some viruses

A

• These 2 viruses have similar antigens so if you develop immunity against cow pox you develop immunity against smallpox

antibody targeting one will eradicate both

  • But most viruses have no non-pathogenic antigenically related counterpart
  • Antigenic variability of small pox is very limited therefore vaccines are effective. Unlike vaccines against influenza in which there is great variability
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9
Q

what are the Features of effective vaccines

A
  • Safe, protective, gives sustained protection, induces neutralising antibody, induces protective T cells and considers practical considerations (low cost per dose/ few side effects & ease of administration). Must be economically viable.
  • The best vaccine will activate both arms of the immune response
  • Must elicit t-cell response as then t-cell response is weak and won’t be sustained
  • Many pathogens require t-cells to remove them (t-cell immunity)
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10
Q

outline some Infections with no completely effective vaccines

A
  • Issue Is there is no effective immune response
  • Malaria, tuberculosis, cholera, HIV, seasonal flu and measles.
  • Measles - vaccine must be refrigerated to be effective, therefore difficult to get to parts of Africa.
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11
Q

outline the methods vaccination can be based on

A

Vaccines based on killed organisms

Vaccines based on attenuated organisms

Production of recombinant vaccines

conjugate vaccines

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12
Q

outline how Vaccines are based on killed organisms and what are the risks of this

A
  • Chemically treated, heated or irradiated - viruses cannot replicate however may contain antigenic potential. Essentially neutralising it (removing ability to replicate).
  • These viruses have nucleic acids susceptible to damage – irradiate it with UV light, or heat it
  • Need large quantities of virus for vaccine
  • Danger of infection due to inefficient killing e.g. Salk polio vaccine  accidentally inoculating individual with pathogen
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13
Q

outline the process of Selection of attenuated viruses for use as vaccines

A

Empirical selection of non-virulent ‘live-attenuated’ organisms (by experiment)

Grow cells in the lab, culture the virus (need live cells), culture until you get a strain that will replicate but not cause disease- attenuated with respect to its ability to cause disease. - virus no longer grows well in human cells
• Live, attenuated virus will not cause disease however will confer resistance
- Mimics the natural type of infection but does not cause any pathology
• No damage caused  virus cannot replicate in human cells

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14
Q

outline examples of Vaccines based on attenuated organisms

A
  • Measles, mumps, rubella, Sabin polio vaccine (viruses)
  • BCG vaccine for TB but level of protection highly variable: 50-80% in UK (effective protection in children but not adults)
  • Salmonella typhi vaccine (typhoid fever)
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15
Q

outline features of Immune responses and live-attenuated vaccines

A
  • Mimic natural infections in terms of interaction with immune response
  • Better (long-lasting) immunity
  • Not virulent as not presented by class I MHC
  • Elicit CD4+ T-cells as well as CD8+ T-cells
  • Inactivated viruses cannot produce cytosolic virus particles therefore can’t be presented with MHC class I
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16
Q

outline examples of Diseases caused by bacterial toxins:

A

• Some vaccines are available against some of these. These vaccines comprise of inactivated toxins e.g. DTP – Diptheria, Tetanus, Pertussis

17
Q

outline the Production of recombinant vaccines and what vaccine is made that way

A
  • Hepatitis B made this way
  • Requires knowledge of the chemical properties of the pathogen
  • Remove gene that encodes antigen
  • Produce hepatitis B surface antigen
  • Insert into yeast (lots produced quickly)
  • Eukaryotic  sophisticated method of modifying proteins i.e. glycosylation
18
Q

outline how vaccines comprising of a specific polysaccharide antigen can be used against encapsulated bacteria

A

Encapsulated bacteria are difficult to develop vaccines against

requires a good complement response, specifically the classical pathway as this involved antibodies- alternative pathway is not sufficient

Capsular subunit vaccines (comprising purified specific polysaccharide antigen) give rise to a thymus independent immune response (no T cells made)

Thus Only IgM made, no class switching, no somatic hypermutation, no memory

This provides protective immunity in adults but not in children and the elderly (who require helper T-cells to activate B-cells-’linked recognition’)

19
Q

outline Examples of conjugate vaccines

A
  • Haemophilus influenzae type b (meningitis & serious chest infections)
  • Neisseria meningitides serogroup C (meningitis)
    (Meningitis is not one disease, it’s a symptom of many diseases (including measles)
20
Q

outline how Conjugate polysaccharide vaccines are a more potent vaccine.

A
  • Toxin promotes t-cell response
  • Amplifies normal immune response
  • Conjugate vaccines have specific polysaccharide antigen chemically coupled to carrier protein e.g. tetanus toxin
  • This converts the polysaccharide to a T-dependent antigen
  • Stimulates CD4 T-cell response and hence B-cell help for a more effective vaccine
  • Several experiments done and select the one with best immune response
  • Conjugate a polysaccharide antibody will allow a more effective immune response
  • Conjugate better than polysaccharide
21
Q

outline how the Route of vaccination is an important determinant for vaccine success

A

• Many important pathogens enter via mucosal surfaces
• Most vaccine given by injection not by mucosal route
Except e.g. intra-nasal ‘flu vaccine (children only); oral polio vaccine (better immune response if injected)
• Injections induce systemic antibodies which may not prevent all disease symptoms responses
• Mucosal immunisation induces mucosal antibodies which are more effective against the disease
• Injected – destroyed in stomach otherwise
• Practical disadvantages - risk of infection/ requires skilled staff/ cost/ discomfort

22
Q

what are Adjuvants

A

other substance which stimulates the immune system before the pathogen enters (squalene/ oil/ aluminium salts). Add to formulation of vaccine to make them work better

  • Purified pathogen antigens do not elicit a good innate immune response
  • Needed to activate immune responses e.g. APC to stimulate T-cells
  • Substances added to vaccines to encourage inflammation
  • E.g. ‘alum’ (aluminium salts), bacterial components of combination vaccines (e.g. B. pertussis toxin component of DTP), oils e.g. squalene
  • Induces sterile inflammation (interact with NLR e.g. uric acid crystals will act with NLR causing gout)
  • Mimics what happens naturally in infections
23
Q

outline the distribution of of immunoglobulin isotypes between mother and child

A

passive immunity

Dimeric IgA – mucosal surfaces. Passed through in breast milk

Monomeric IgA goes around serum

IgG – protects most tissues

  • Developing baby is protected by IgG passively
  • IgG crosses placenta, IgM doesn’t cross the placenta as its too large

IgE – allergic reactions

IgA- After birth, child protected by IgA (mucosal) in mother’s milk

24
Q

outline The development of immune responses in man

A
  • IgM has 5 antibody molecules stuck together  difficult to get across placenta
  • IgG can easily cross the placenta
  • Premature babies even more vulnerable because their immune system is behind. Babis still very susceptible until around 7 months when immune system starts to kick in
25
Q

outline how passive immunity is attained in new borns as adaptive immunity does not fully function until 6 months post-partum

A
  • IgG across the placenta-in utero and post-partum protection
  • IgA from mother’s milk passive immunisation against gut pathogens
  • Babies (and especially premature babies) are susceptible to infection- behind in bone marrow/immune system development
  • Also n.b. (horse) antisera to snake and spider venom (and previously bacterial toxins e.g. tetanus)  provides passive immunity. Rare event so no vaccines
26
Q

outline The principle of herd immunity

A

if most of the population have protective immunity, then the susceptible minority are protected (nowhere for pathogen to go).
• Protects community
• Limited potential for pathogen to thrive in individual
• Mirco-organism has a low probability of finding non-immune host
• Chain of infection not created
• The more non-immune people in a population, the greater the likelihood of outbreaks and epidemics
• Therefore: routine childhood immunisation programme
• We are no longer measles free as threshold is 85-90%

27
Q

hw can measles spread and what are symptoms

A

droplets in coughs and sneezes

cold-like symptoms, fever, tiredness, kopliks sports

28
Q

what is an early sign of measles infection in the oral cavity

A

Koplik’s spots

29
Q

outline the features of Measles and the MMR vaccine

A
  • Measles vaccine introduced in 1968, MMR in 1988.
  • MMR is combination vaccine- works better
  • Average 100 deaths every year in the UK before the vaccine. 13 per annum before MMR.
  • Deaths occur in unimmunised children and leukaemia patients in remission (immunosuppressed)
  • Young people born between 1998/00 and 03/04 are most succeptive
  • They go to festivals and university
  • Uptake in 2016 & 2017 of first vaccine dose >95% but currently only 88% for the second
  • New UK measles and rubella elimination strategy for 2019
30
Q

iah 20 flashcards are in theme 2

A

so annoying i know

Stage 2 (16 decks)

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