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AQA A Level Biology > 3.2 Chapter 5- Immunity > Flashcards

3.2 Chapter 5- Immunity Flashcards

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1
Q

What are interactions between different types of cell involved in?

A

Disease, recovery from disease and prevention of symptoms occurring at a later date.

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2
Q

How does immunity prevent symptoms upon reinfection?

A

If exposed to the same antigen, or antigen-bearing pathogen, this generates a faster immune response.

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3
Q

What happens if a pathogen overwhelms defences?

A

Death

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4
Q

How does immunity work?

A

1.Defence mechanisms overwhelm the pathogen leading to recovery.
2. The body is better prepared for the 2nd infection and kills the pathogen before harm occurs.

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5
Q

What is the first defence mechanism?

A

Primary defence (skin, physical and chemical defence)

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6
Q

What is the second defence mechanism?

A

Secondary defence (White blood cells)

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7
Q

What do phagocytes respond to, what are the features of this response and how do they work?

A

General pathogens- non-specific
Immediate response.
Ingest and destroy pathogen.

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8
Q

What do T cells respond to, what are the features of this response and what is that response called?

A

Respond to specific pathogens
Longer lasting response
Cell mediated Immunity

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9
Q

What is the response of B lymphocytes called?

A

Humoral response

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10
Q

What are T lymphocytes and B lymphocytes an example of?

A

Specific defence mechanisms.

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11
Q

What are physical barriers and phagocytes an example of?

A

Non- specific defence

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12
Q

How many different types of lymphocytes are there and why?

A

Tens of millions
To recognise different antigens

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13
Q

How do lymphocytes develop in the foetus?

A

The foetus rarely gets infected as protected by placenta which acts as a barrier to infection.
The mother provides antibodies to the foetus from the placenta.
Foetuses lymphocytes collide almost only with own cells and if they generate an immune response they die or are supressed.
The remaining lymphocytes are for non- self material- respond to foreign antigens.

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14
Q

How are lymphocytes developed in adults?

A
  1. Formed in the bone marrow where they only encounter self antigens.
  2. If shows an immune response to them- undergo programmed cell death before differentiate into mature lymphocytes.
  3. No clones appear in the blood- only non-self recognising lymphocytes.
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15
Q

When are lymphocytes not formed?

A

In response to an infection- already exist.

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16
Q

Why does the large number of lymphocytes help the immune response?

A

10s of millions
So many- when an infection occurs high probability already at least one lymphocyte will have a complementary receptor to the pathogens antigen protein and recognise it.

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17
Q

What does the large number of lymphocytes mean there are?

A

Few numbers of each type of lymphocytes.

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18
Q

How does the small number of each type of lymphocyte impact the immune response?

A

Causes clonal selection.
The small numbers of lymphocytes complementary to the pathogen have to come into contact with the pathogen and divide and build up so they can destroy the pathogen.
Causes a time lag.

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19
Q

What is an antigen?

A

A foriegn (non-self) protien that stimulates an immune responce.

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20
Q

What are antigens often in the form of and what is their role?

A

Proteins embedded within the membrane that allow recognition of self and foreign cells by the immune systems.

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21
Q

What can also be another form of antigen?

Hint: Begins with T

A

Toxins produced by bacteria

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22
Q

What is the difference in the response to foreign (non-self) antigens and to self antigens and why?

A

Foreign antigens trigger an immune response.
Self antigens do not trigger an immune response.
Otherwise white blood cells would attack the organisms own cells

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23
Q

Why are antigens often proteins?

A

Proteins have a large variety of specific tertiary structures.

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24
Q

What do antigens enable the immune system to identify?

Hint: 5 points

A
  • Pathogens- e.g. bacteria
  • Abnormal body cells- cancerous or pathogen infected
  • Toxins- poisonous molecules- often released by bacteria
  • Cells from other individuals of the same species.
  • Cells infected by a virus
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25
Q

Why is the immune system recognising cells from a different organism of the same species problematic?

A
  • Not good for transplants
    e.g. organ/ blood transplant
    Transplants often destroyed- rejected by immune system.
  • To minimise rejection- transplants genetically matched as close as possible and immunosuppressant drugs are taken.
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26
Q

What is a phagocyte?

A

A type of white blood cell that performs phagocytosis. Often either a neutrophil or a macrophage.

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27
Q

What is phagocytosis?

A

Engulfment of large particles e.g. bacteria in vesicles formed by the cell surface membrane.

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28
Q

Where are phagocytes found?

A

In blood and tissue fluid. Move from the blood vessels and transported into tissue fluid.

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29
Q

Describe phagocytes role/ response?

Not to do with phagocytosis

A

Defend against pathogens that enter the body. First cells to respond to the immune system trigger fast. Non- specific response.

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30
Q

Describe the process of phagocytosis

Hint: 7 steps

A
  1. Chemical products of non-self cells attract phagocytes.
  2. The phagocyte recognises the foreign antigen and attaches to it with receptors.
  3. Engulfs pathogen or non-self material (surrounds by cell membrane) forming a vesicle called a phagosome.
  4. Lysosomes fuse with vesicle
  5. Lysozymes- hydrolytic enzymes- hydrolyse/ break down/ digest the pathogen e.g. hydrolysis of the bacterial cell wall.
  6. Soluble products absorbed into the cytoplasm. Indigestible material removed.
    7.The phagocyte presents the antigens on the cell membrane to activate other immune system cells. Becomes an antigen presenting cell i.e a macrophage.
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31
Q

What response do T Lymphocytes produce?

A
  • Cell mediated responce
  • Specific- respond to specific antigens
  • Slow but long lasting
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32
Q

What type of cells can T lymphocytes be?

A
  • Helper T cells
  • Cytotoxic T cells
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33
Q

How are T lymphocytes produced?

A
  • Produced in the bone marrow.
  • Mature in the thymus
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34
Q

What do T Cells respond to?

A

Respond only to antigens on abnormal body cells- cell mediated immunity:
1. Organisms own cells that have been infected by non-self material e.g. Cells invaded by a virus presenting virus antigens.
2. Antigen presenting cells. Often foriegn antigens from phagocytes presenting antigens on the cell surface membrane.
3. Cells of different organisms from the same species.e.g. transplanted cells presenting different antigens on their cell- surface membrane
4. Cancer cells displaying different antigens- tumour markers

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35
Q

What are cells displaying foriegn antigens called and where do they present antigens?

A

Antigen presenting cells.
Present antigens on cell surface membrane.

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36
Q

What type of response do T lymphocytes create.

A

Cell mediated immunity/ a cellular response.

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37
Q

How are T lymphocytes activated?

A

Receptor proteins on surface bind to a specific complementary antigen on antigen presenting cells e.g. phagocytes activating it.

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38
Q

Why are there vast numbers of T cells?

A

Respond to a single antigen.
Each for a different antigen so many different types.

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39
Q

Describe the helper T cells responce:

Hint: 3 steps.

A
  1. Receptors on specific helper T cells bind to antigens on antigen presenting phagocytes.
  2. This activates the T cell- divides rapidly by mitosis and forms clones
  3. The cloned T cells can then become:
    a. Helper T cells that release chemical signals that stimulate B cells to clone and form plasma cells that secrete antibodies.
    b. Develop into memory cells and stimulate a rapid responce to future infections of the same pathogen.
    c. Helper T cells that release chemical signals that activate and stimulate phagocytes to perform phagocytosis
    d. Helper T cells that activate cytotoxic T cells.
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40
Q

What happens when T cells are activated?

A

They are cloned by mitosis (clonal selection).

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41
Q

What can T cells become after they are activated?

A
  1. Memory cells- activate B cells and create a rapid response to future infection.
  2. Helper T cells- release chemical signals that activate and stimulate phagocytes to perform phagocytosis or specific B cells to secrete antibodies
  3. Cytotoxic T cells
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42
Q

What do Cytotoxic T cells do?

A

Kill abnormal body cells and cells infected by pathogens.

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43
Q

How do cytotoxic T cells perform their role?

A
  1. Produce perforin protein
  2. Makes holes in cell- surface membrane.
  3. Membrane becomes permeable to all substances, water and ions enter the cell by osmosis/ diffusion and the cell can no longer function and is destroyed. (demostrates membranes importance).
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44
Q

What are Cytotoxic T cells most effective against?

A

Viruses as they replicate inside cells.

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45
Q

Why are body cells sacrificed by Cytotoxic T cells.

A

To prevent viral replication.

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46
Q

What type of immunity do B cells produce and why is it called this?

A

Humoural immunity- antibodies soluable in blood and tissue fluid.

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47
Q

Describe the features of humoural immunity.

A
  • Specific, slow responce
  • Long term immunity
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48
Q

How are B cells produced?

A

By stem cells in the bone barrow. Mature in the bone marrow.

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49
Q

Why are there many different types of B cell?

A
  • Large variety of antigens but only one type of B cell is complementary to each antigen.
  • Each B cell has a different antibody complementary to antigens to form antigen- antibody complexes.
  • Ensures there is at least one complementary B cell to every type of antigen.
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50
Q

Describe the structure of a B cell:

A

Covered in antibodies on their membrane- each cell has different specific antibodies.

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51
Q

Describe clonal selection in B cells (the main type):

A
  1. The antibody on a B cell binds to the complementary antigen.
  2. The antigen is processed- enters to B cell and gets presented on the B cells surface.
  3. T Helper cells bind ot the processed antigens and stimulate B cells to divide by mitosis and clone into identical B cells that may become plasma cells or memory cells. Each produces an antibody specific to the antigen.
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52
Q

How does clonal selection help immunity?

A

Produces a rapid response and a large number of antibodies in response to infection.

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53
Q

What type of antibodies do B cells produce?

A

Monoclonal antibodies- a single type of antibody specific to the antigen.

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54
Q

Describe what plasma cells do and the features of what they do (in detail).

A

Secrete antibodies into blood plasma. Last only a few days but secrete many antibodies complementary to the antigen to form antigen- antibody complexes and prepare the antigen and pathogen for destruction.

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55
Q

Describe the features of memory cells.

A
  • Long living
  • Provide long term immunity.
  • Circulate in blood and tissue fluid.
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56
Q

Name and describe the response of memory cells:

Hint: 5 steps

A

The secondary immune responce:
1. Memory cells encounter the same antigen the B cells defeated before.
2. Memory cells divide rapidly and develop into plasma cells and more memory cells.
3. The plasma cells produce antibodies to destroy the pathogen.
4. A higher concentration of antibodies is secreted and faster than the primary responce. This ensures the infection is destroyed before any harm or symptoms occur.
5. The new memory cells circulate ready for future infection.

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57
Q

What is the first production of plasma and memory cells an example of (and describe)?

A

A primary immune responce- the first immediate responce to an infection.

58
Q

What produces the secondary immune responce?

A

Memory cells.

59
Q

Describe how B cells work:

(Hint- 6 steps)

A
  1. When the B cell comes into contact with its specific pathogen the antibodies on the surface bind to the complementary antigens
  2. The antigens on the surface of the pathogen are taken up by the B cell, processed and presented on the B cells surface membrane.
  3. An activated helper T cell binds to the antigen on the B cells surface receptor and stimulates B cells to divide by mitosis and clone itself- clonal selection.
  4. The cloned B cells develop into either plasma cells or memory cells.
  5. The cloned plasma cells secrete a specific complementary antibody to the pathogens antigen. This antibody attaches to the antigens on pathogens and helps to destroy them.
  6. The memory cells stay in the blood to respond to future infections in the secondary immune response by dividing rapidly and forming plasma cells if the same pathogen is detected.
60
Q

Describe what antibodies are made of:

A

Protiens made of 4 polypeptide chains of sequences of amino acids that form a primary strucure and a specific 3D tertiary structure. Disulfide bridges then form a quanternary structure joining 4 polypeptide chains together.

61
Q

How are antibodies made?

A

Synthesised by B cells

62
Q

Describe the structure of antibodies.

Hint: 6 points

A
  • Two specific identical binding sites complementary to the specific antigen to form antigen antibody complexes. Specific to the antigen.
  • Made from 4 polypeptide chains joined together by disulfide bridges to form the quanternary structure.
  • 2 long heavy chains in a pair at the base of the antibody that form the constant region- same in all antibodies. Binds to B cells on receptors.
  • 2 short light chains in a pair at the top that form the variable region that antigens bind to- two binding sites- one on each chain. The binding sites are different on different antibodies. Each has a specific sequence of amino acids and tertiary structure- 3D shape that binds to the complementary antigen.
  • Lots of disulfide bridges hold the antibody together to make it strong
  • Has a hinge region ot make it flexible upon antigen binding.
63
Q

How do antibodies have so much variety?

A

Wide variety of protien structure enables variety in the variable region.

64
Q

What do antibodies not do?

A

Destroy antigens- they instead prepare them for destruction.

65
Q

What roles do antibodies have?

(Basic roles)

A
  • Agglutination
  • Stimulating phagocytosis
  • Neutralising toxins
66
Q

Describe agglutination.

A
  • Mainly for bacteria
  • Antibodies bind to two antigens at a time
  • Causes the pathogens to clump together
  • Makes it easier for phagocytes to locate and engulf the pathogen
  • Disables the pathogen and makes it less effective as it is unable to move as easily
67
Q

How do antibodies stimulate phagocytosis?

A

Stimulates phagocytes to engulf pathogens especially bacteria.
- Bind to the antigen
- ‘Mark’ and attract phagocytes to the pathogen
- Act as binding sites for the phagocyte to attatch to making the pathogen easier to engulf (opsonisation)

68
Q

How do antibodies neutralise toxins?

A
  • Bind to them and make them harmless
  • Bind to the toxin and cause a phagocyte to destroy it
69
Q

Why can antibodies sometimes be bad for your own body cells?

A

Can sometimes bind to antigens on body cells with a similar shape to the antigens to the pathogen, causing the destruction of the body cell.

70
Q

Describe the primary immune response.

A
  • Occurs when an antigen first enters the body and activates the immune system.
  • Slow- not many B cells to make the antibodies but eventually makes enough antibodies to overcome the infection.
  • Symptoms occur
  • T and B cells produce memory cells that stay in the body for a long time and recognise the specific antigen the second time around. These record the specific antibodies needed to combat the antigen and respond quickly to the second infection.
  • Involves clonal selection of B cells to plasma cells to release antibodies
  • The person becomes immune
71
Q

Describe the secondary immune responce.

A
  • The same pathogen as before infects the body
  • Memory T and B cells circulate in tissue fluid and blood and encounter the pathogen. Clonal selection occurs faster.
  • B cells are activated and divide rapidly into memory cells and plasma cells that quickly produce the right antibody.
  • Memory T cells are activated and divide into the correct type of T cell that kill antigen carrying cells
  • Antibodies released at a faster rate and at a higher concentration.
  • No symptoms, harm or side effects
  • Stronger immune response
  • New memory cells produced further increasing the immune response if a third infection occurs
72
Q

What is the cellular/ cell mediated immune responce?

A
  • T cells and the other immune system cells they interact with e.g. phagocytes.
  • Response to organisms own cells that are infected or cancerous
  • Response to cells from individuals of the same species
73
Q

What is humoural immunity?

A

Named after antibodies being soluable in fluid. Involves:
* B cells
* Clonal selection
* Monoclonal antibodies

74
Q

Why are both humoral and cell mediated responses important?

A
  • Both needed to remove the pathogen from the body
    All interact with each other:
  • T cells activate B cells.
  • Antibodies activate phagocytes
75
Q

What might you need to mention when interpreting data surrounding vaccines/ medications/ infections?

A

May need to identify whether a response is primary or secondary and suggest evidence to back this up.

76
Q

Draw the primary and secondary immune response graph.

A

Answer on revision card.

77
Q

Describe active immunity.

A
  • Produced by stimulating antibody production from plasma cells
  • Antibody produced in reponse to antigens
  • Long term response- memory cells produced.
  • Slow to develop
  • Performed by the individuals own immune system
78
Q

What are the two types of active immunity?

A
  • Natural active immunity- when infected by a disease, body produces its own antibodies
  • Artificial active immunity- vaccination, induced immune response.
79
Q

Describe passive immunity.

A
  • Antibodies introduced to the body from an outside source
  • No contact with the antigen needed
  • Immediate and fast acting response
  • No memory cells
  • Short term immunity as antibodies not replaced when broken down
80
Q

What are the two types of passive immunity?

A
  • Natural- babies antibodies from mothers placenta and breastmilk
  • Artificial- injected with another organisms antibodies e.g. antivenom.
81
Q

What language must you remember to use when comparing?

A

Comparitive language e.g. more/less/faster

82
Q

What is a vaccination?

A

Introduction of antigens into the body through injection or mouth to stimulate an immune response from white blood cells.

83
Q

Where do antigens come from in vaccination?

A
  • Free or attatched to a dead or inactive pathogen
  • For a virus- sometimes use genetic material- introduces the genome and proteome and therefore the antigens
84
Q

What is the simplified order of an immune responce to a vaccine?

A

Pathogen-> T cell -> B cell -> plasma cells and memory cells-> antibodies

85
Q

How are the side effects of a vaccine kept to a minimum?

A

Introduce a small amount of antigen to induce a small immune response with limited symptoms.

86
Q

How do vaccines provoke a bodily reaction that creates immunity and a better reaction to a pathogen?

A
  • B cells clone by mitosis and produce plasma and memory cells.
  • Memory cells stay in the blood for a secondary immune response
  • The secondary immune response is more effective- immediate, quicker, higher concentration of antibodies and rapid antibody production.
  • Few symptoms occur
87
Q

How do booster vaccines aid the effectiveness of the vaccine?

A
  • Increase chance of effectiveness of vaccine
  • Produces a secondary response
  • Creates more memory cells
88
Q

Why may vaccines not eliminate disease?

Hint: 8 points

A
  • Fails to introduce immunity e.g. in those with limited immune system
  • Individuals may not develop enough immune responce and infect others
  • Mutations- if frequent in the pathogen tertiary structure of the antigen may change - immune system can’t produce the right antibody to destroy the pathogen.
  • Antigenetic variablility- mutations change antigens frequently- immunity short lived
  • Many variants- may not be effective against all
  • Pathogen can ‘hide’ inside cells/ out of reach in places e.g. intestines
  • Individuals may object- religious/ moral/ medical grounds
  • Oral vaccines- antigens can be broken down by digestion/ may be too large to be absorbed.
89
Q

What must you be careful about when looking at antibody production when a vaccine is given?

A

Antibodies decrease over time as they are broken down.

90
Q

What must successful vaccines be?

Hint: 5 points

A
  1. Economically viable- available in enough quantities to be made cheaply
  2. Few side effects- bad ones may discourage/ negatively impact people
  3. Available means of storing, producing and transporting the vaccine- technology and hygine
  4. Means of administering the vaccine- staff with the appropriate skills
  5. Herd immunity must be achievable
91
Q

What must you remember when describing vaccines?

A

Describe the B cells and T cells response.

92
Q

Describe how the body responds to vaccines.

Hint: 8 steps

A
  1. Vaccines contain antigens/ protiens/ genetic material to make antigens from the pathogen
  2. Phagocytes/ macrophages engulf and present antigen
  3. T cells with complementary receptor protiens bind to the antigen and are activated
  4. B cells bind to the complementary antigen. T cells stimulate B cells with complementary antigens.
  5. B cells clone by mitosis resulting in the clonal selection of specific B cells
  6. B cells produce plasma cells that secrete antibodies against the antigen and some B cells become memory cells
  7. On the second infection the memory cells produce plasma cells and antibodies faster so that the infection is quickly contained and no symptoms occur.
  8. The second infection causes more memory cells to appear in your blood- stay and produce antibodies quicker on reinfection of the same antigen presenting pathogen.
93
Q

What is herd immunity?

A
  • Occurs when a sufficiently large proportion of the population is vaccinated so it is difficult for the pathogen to spread.
  • When most of the population is immune it is less likely that those who are not immune will come into contact with the pathogen.
  • Protects those that aren’t immune.
94
Q

Why is herd immunity important?

A

Important as not possible to vaccinate everyone e.g. the vulnerable, immunosuppressed.

95
Q

How many people should be vaccinated to achieve herd immunity and when should they be vaccinated.

A
  • The percentage needed is different for each disease
  • Best to vaccinate at the same time
96
Q

What ethics must be considered with regard to vaccines?

Hint- 11 points

A
  • Who will be the first to recieve the vaccine
  • Animal testing/ use of animal parts
  • Expense- especially if little chance of infection
  • Side effects- do benefits outweigh risks and do side effects cause long term harm
  • Testing- when first trialling on humans- coud be risky and compromise health
  • Unfair if some people have access to the vaccine and others don’t
  • To achieve herd immunity- how many people need to be vaccinated?
  • Should it be compulsory to have a vaccination?
  • People may opt out due to beliefs, religion or medical reasons
  • Balancing health risks of a few individuals vs the health of a majority
  • Should we continue to use a vaccine if the disease is almost eliminated
97
Q

What must you do when looking at vaccine data?

A
  1. Discuss the efficacy of the vaccine e.g. in herd immunity, effectiveness after one dose.
  2. Use data and describe what it shows
98
Q

What are monoclonal antibodies?

Hint: short definition

A

Antibodies with the same tertiary structure.

99
Q

How are (monoclonal) antibodies specific to their antigen?

A

They have a binding site with a unique complementary tertiary structure.

100
Q

How can monoclonal antibodies be produced?

A
  • Naturally from genetically identical cloned B cells within the body
  • Artificially outside of the body for medical and scientific use
101
Q

What are the uses of artificially produced monoclonal antibodies?

A
  • Targetting drugs to specific cells/ antigens
  • Blocking antigens/ receptors on cells
  • Medical diagnosis
102
Q

How do monoclonal antibodies target drugs to specific cells/ antigens?

A
  • Also known as indirect monoclonal antibody therapy
  • As specific to antigen only target one cell e.g. cancer cells that have tumour markers that are different from normal cells
  • Bind to the cells e.g. tumour cells and target drugs to kill the cell e.g. radioactive substances
103
Q

What is the advantage of using monoclonal antibodies to target drugs?

A

Less side effects as the drug doesn’t target normal cells.

104
Q

How do monoclonal antibodies stop cells from being harmful apart from targetting drugs to them and what is the advantage of this method?

A
  • Block antigens/ receptors on cells
  • Bind to specific antigens e.g. tumour markers
  • Block chemical signals getting to the cell e.g. growth signals that cause uncontrolled growth
  • Fewer side effects
105
Q

How are monoclonal antibodies used to diagnose disease? Give e.g.s

A
  • Diagnose diseases e.g. prostate cancer rapidly
  • The antibodies diagnose diseases by binding to their antigens
  • Used in the ELIZA test
106
Q

What does a diagnosis with monoclonal antibodies usually require afterwards?

A

Further investigation as not always accurate

107
Q

Describe how pregnancy tests work.

Hint: 7 point

A
  • Pregnancy tests detect Human Cholionic Gonadotropin (hCG)- produced by the placenta during pregnancy and found in urine
  • The application area contains antibodies complementary to the hCG antigens bound to coloured particles
  • If the hCG is present in the urine it will bind to the antibody forming an antigen-antibody complex. The hCG will then move down the test strip with the urine carrying the antibodies and colour.
  • The test strip contains antibodies to hCG that are held in place.
  • If the hCG is present then the strip turns coloured- immobilised antibody binds to the hCG concentrating the hCG- antibody complex.
  • If no hCG is present the antibodies and the colour pass through the test area without binding and don’t turn blue.
  • Once the control is reached all remaining antibodies bind to more fixed antibodies creating another line.
108
Q

What ethical issues are there surrounding monoclonal antibodies?

Hint: 6 points

A
  • Mice are used to produce antibodies and animal tumour cells- animal rights concern. Animals are sometimes monitored to avoid suffering
  • Animals may be tested on the drug causing a reaction and death, animals are sometimes monitored to avoid suffering
  • Risk of side effects including death in the treatment of multiple sclerosis
  • Important that patients know risks vs. the benefit and give informed consent
  • Testing of the drug can pose risk to humans e.g. organ failure
  • Enough knowledge should be available that people feel free to make informed decisions
109
Q

When do antigens activate a secondary immune response?

A

If they are the same

110
Q

What is antigenetic variability?

A

When a pathogens antigens change- causes variation.

111
Q

What is the effect of antigenetic variability on immunity?

A
  • Memory cells don’t recognise the second infection or produce the right antibodies for it
  • A primary immune response has to occur
112
Q

What is antigenetic variation caused by?

A
  • Mutations in RNA/DNA/genetic material
  • Causes a new primary and tertiary structure
  • Results in new antigens that are no longer recognised by the immune system so antibodies for the pathogen are not made quickly
113
Q

What effect does antigenetic variation have on vaccines and give an example?

A
  • Makes vaccines inneffective
  • Makes it hard to develop vaccines against pathogens that mutate frequently e.g. influenze, HIV
  • As the flu’s antigens change every year the previous vaccine becomes innefective and a new vaccine has to be made every year
114
Q

What effect does antigenetic variation have on pathogens especially viruses?

A
  • Mutations in DNA lead to changes in tertiary structure of attatchment protiens of viruses
  • Leads to pathogens or viruses being able to attack other species
115
Q

Why are different species antigens used in different treatments and name which type of treatment?

A
  • Different species antigens used in different antibody treatments
  • Each species has different forms of antigens- due to mutations leading to different tertiary structures
  • Different complementary antibodies are needed to combat this
116
Q

What do theories need to be tested with? and give an example

A
  • Evidence to reject or confirm them
  • Repeats or reproductions of tests
  • e.g. the MMR study suggested vaccine cause autism. Very unlikely- small sample size, bias due to being paid by parents in a legal case. Undermined by a Japanese study of a much larger sample showing no correlation. However, still led to some parents being skeptical
117
Q

How should we judge data?

A
  • Data should be judged critically
  • Correlation does not equal causation
  • Consider bias, new evidence and peer reviews
118
Q

How should we answer questions about data? Give an e.g.

Hint: 4 points

A
  1. Describe the data e.g. continued to rise after…, AIDs slowed after…
  2. Explain what the data shows e.g. primary or secondary immune response, whether the pathogen is still affecting the person
  3. Evaluate methods e.g. confident as a large sample size
  4. Draw conclusions e.g. correlation or lack of correlation
    e.g. Herceptin- monoclonal antibody drug used to treat breast cancer. Tested with a control group who did not have the drug
    Describe the data e.g. 2x died as those with Herceptin
    Conclusion- treatment with Herceptin increases the survival rate.
119
Q

What should you mention when evaluating drugs?

Hint: 8 points

A
  • Give positives and negatives
  • Use data to back up your answer
  • Discuss the safety- whether it has been tested on animals/ humans/ tested repeatedly
  • Discuss the efficacy of the drug- at what concentration is it effective, how many doses, does it work on only one type of pathogen, how long do the effects last
  • Is another factor influencing the results- is there a control group
  • Consider the limitations of the study- number of people tested on, how long the test was, and whether stats tests were used
  • Consider mutations of pathogens- whether it encourages/ prevents the spread of a resistant diseases
  • Consider the availability of the drug
120
Q

Describe the structure of HIV.

A
  • RNA core and enzymes (reverse trabscriptase)
  • Surrounded by a protien capsid
  • Surrounded by a lipid envelope
  • Attachment protiens embedded in the envelope to help it attach to the host cell
121
Q

What is one of the most important enzymes in HIV, what does it do and what does it relate to?

A

Reverse transcriptase- catalyses RNA into DNA- the reverse of transcription. Why HIV a retrovirus as reverses the process. Needed for HIV replication.

122
Q

How does HIV replicate?

Hint: 7 steps

A
  1. HIV enters the bloodstream and its attatchement protiens attatch to receptors on helper T cell hosts (CCR5 receptor)
  2. The lipid envelope and protien capsid fuse with the cell surface membrane and releases RNA and enzymes
  3. The reverse transcriptase converts RNA to DNA
  4. Another DNA strand is made to make the viral DNA doube stranded.
  5. The new DNA moves into the hosts nucleus and inserts into the cells DNA
  6. The host cells enzymes are used to produce viral protiens, enzymes and RNA. This works by producing mRNA from transcription that is translated into protien in protien synthesis producing the protiens and RNA for HIV.
  7. The viral protiens are assembled into new viruses. The HIV breaks away from the T cell with a piece of it’s cell-surface membrane forming it’s lipid envelope.
  8. The HIV is released and is able to infect other cells.
123
Q

What illness does HIV cause?

A

AIDS- a condition where the immune system deteriorates and fails.

124
Q

How does HIV cause AIDS?

Hint: 6 points

A
  1. Attacks helper T cells destroying them or making them non-functional
  2. Leads to critically low T cells
  3. Memory cells are also infected and destroyed
  4. Fewer T cells to stimulate B cells or cytotoxic T cells. B cells don’t undergo mitosis.
  5. Less/ no antibodies produced as B cells don’t become plasma cells
  6. The body is unable to produce an immune response- susceptible to cancer and infections
125
Q

What kills a person with AIDS?

A

AIDs lead to critically low T cells
The secondary diseases e.g. pneumonia.
HIV doesn’t kill individuals directly but inhibits their immune system causing AIDS

126
Q

When does HIV turn into AIDS and what happens?

A

Around 10 years after first infection.
Initially minor infections then respiratory infections then severe infections that vaccines would usually protect against.

127
Q

What happens after HIV initially infects somebody?

A
  • Replicates rapidly and flu like symptoms occur
  • Then replication drops and the HIV lies dormant and latent for years. Lives within cells and no symptoms develop
128
Q

How do antibiotics work against bacteria?

A
  • Antibiotics kill bacteria by destroying their cell wall meaning the bacteria can’t survive
  • Water constantly enter the bacterial cells by osmosis and the cell is stopped from bursting by the murein cell wall being not easily stretched- the cell membrane pushes against it but the wall resists expansion and stop the water from entering the cell
  • Antibiotics inhbit the enzymes and metabolic reactions used to build the cell walls- especially the cross linkages
  • This weakens the cell wall so it cannot withstand the water pressure and the cell bursts and dies
129
Q

How do antibiotics kill bacterial cells but not human cells?

A

Inhibit enzymes/ structures within the bacteria specific to the bacteria but not human cells
Inhibit structures with a different tertiary structure to human structures e.g. a different shape active site
The antibiotic is not complementary to human structure

130
Q

Why do antibiotics not work against viruses?

A

Viruses use the host cells metabolic pathway.
* Antibiotics are useless as they usually inhibit metabolic processes or stuctures but there are none to disrupt as the virus uses the cells features.
* Viruses have a protien capsid not a cell wall so the antibiotics don’t work
* If a virus is within a cell the antibiotic wouldn’t reach them
* Antibiotics target enzymes and ribosomes- only bacterial as humans are different. Viruses don’t have enzymes and ribosomes and use thier hosts. Antibiotics can’t inhibit human processes.

131
Q

How do antivirals work?

A

Target virus- specific enzymes e.g. reverse transcriptase inhibitors for HIV

132
Q

What is the cure for HIV?

A
  • HIV doesn’t have a definitive cure.
  • The best prevention of HIV is to stop body fluid tansfer
  • Antivirals can be used to prevent spread- some inhibit reverse transcriptase to stop HIV forming. However DNA of old infected cells still affected so HIV still made.
133
Q

What is the role of the ELIZA test?

A

Tests if a patient has antibodies to an antigen or the antigen itself.

134
Q

What are the properties of the ELIZA test?

A

Qualititive and quantitative and sensitive.

135
Q

What can the ELIZA test be used for?

A

Many medical diagnoses including allergies and HIV.

136
Q

What are the types of ELIZA test?

A
  • Direct ELIZA test (unpreffered)
  • Indirect ELIZA test (preffered)
137
Q

Describe the direct ELIZA test (unpreffered method):

Hint: 5 steps

A
  1. Antigens from teh patient are bound to the test and any unbound antigens are washed away.
  2. An antibody complementary to the antigen is added with an enzyme attatched
  3. If the antigen is present the antbody will bind to it and become stuck. The rest of the antibodies are washed away to remove unbound antibodies.
  4. A substrate solution is added
  5. If the antibody is present the enzyme will cause the substrate to change colour giving a positive result. The more enzyme= the more colour change.
138
Q

Describe the indirect ELIZA test (preferred):

Hint: 5 steps

A
  1. HIV antigens attatched to the surface and then the surface is washed to remove unattached antigens
  2. A sample of the patients blood is added
  3. If HIV specific complementary antibodies are present they will bind to the immobile antigen. Any unbound antibodies are washed away.
  4. Add a second antibody with an enzyme attached to it that binds to the first (primary) antibody. Wash to remove unbound secondary antibody. If no primary antibodies- all washed away.
  5. Add a substrate solution that reacts with the enzyme on the secondary antibody. If a colour change- the patient has HIV. More colour= more HIV.
139
Q

What must you not mix up with ELIZA tests?

A

Direct vs Indirect

140
Q

What are the ethical issues of ELIZA tests related to?

A

Monoclonal antibodies

AQA A Level Biology (11 decks)

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