Cell Recognition And The Immune System - Mark Scheme Answers (study Mind) Flashcards

1
Q

Explain why antibody A attaches only to the protein found in species of Plasmodium.

A
  1. Antibody has tertiary structure;
  2. Complementary to binding site on protein.
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2
Q

Explain why antibody B is important.

A
  1. Prevents false negative results;
  2. (Since) shows antibody A has moved up strip / has not bound to any Plasmodium protein.
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3
Q

(a) HSV infects nerve cells in the face (line 1). Explain why it infects only nerve cells.

A
  1. Outside of virus has antigens / proteins;
  2. With complementary shape to receptor / protein in membrane of cells;
  3. (Receptor / protein) found only on membrane of nerve cells.
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4
Q

(b) HSV can remain inactive inside the body for years (lines 2–3). Explain why this virus can be described as inactive.

A
  1. No more (nerve) cells infected / no more cold sores form;
  2. (Because) virus is not replicating.
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5
Q

(c) Suggest one advantage of programmed cell death (line 4).

A

Prevents replication of virus.

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6
Q

The scientists concluded that production of this microRNA allows HSV to remain in
the body for years (lines 10–12).
Explain how this microRNA allows HSV to remain in the body for years.

A
  1. (Binds) by specific base pairing;
  2. (So) prevents mRNA being read by ribosomes;
  3. (So) prevents translation / production of proteins;
  4. (Proteins) that cause cell death.
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7
Q

A mutation of a tumour suppressor gene can result in the formation of a tumour. Explain how

A
  1. (Tumour suppressor) gene inactivated / not able to control / slow down cell division;
  2. Rate of cell division too fast / out of control.
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8
Q

(ii) Not all mutations result in a change to the amino acid sequence of the
encoded polypeptide.
Explain why.

A
  1. (Genetic) code degenerate;
  2. Mutation in intron.
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9
Q

Some cancer cells have a receptor protein in their cell-surface membrane that binds
to a hormone called growth factor. This stimulates the cancer cells to divide.
Scientists have produced a monoclonal antibody that stops this stimulation.
Use your knowledge of monoclonal antibodies to

suggest how this antibody stops
the growth of a tumour.

A
  1. Antibody has specific tertiary structure / binding site / variable region;
  2. Complementary (shape / fit) to receptor protein / GF / binds to receptor protein / to GF;
  3. Prevents GF binding (to receptor).
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10
Q

(a) The scientists gave an injection to a mouse to make it produce the monoclonal
antibody used in this investigation (line 7).
What should this injection have contained?

A

Regulator protein.

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11
Q

(b) LDL enters the liver cells (lines 3−4).
Using your knowledge of the structure of the cell-surface membrane, suggest how
LDL enters the cell.

A
  1. Lipid soluble / hydrophobic
  2. Enters through (phospholipid) bilayer
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12
Q

(c) Explain how the monoclonal antibody would prevent the regulator protein from
working (lines 7−8).

A
  1. (Monoclonal antibody) has a specific tertiary structure / variable region / is complementary to regulator protein
  2. Binds to / forms complex with (regulator protein)
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13
Q

(d) Describe how the control group should have been treated.

A
  1. Injection with salt solution
  2. Otherwise treated the same.
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14
Q

(a) Suggest two reasons why the percentage of infants vaccinated decreased between
1973 and 1975.

A
  1. (Decrease linked to) few(er) cases of whooping cough;
  2. (Decrease linked to) risk of / fear of side effects;
  3. Insufficient vaccine available / too expensive to produce / distribute.
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15
Q

Between 1980 and 1990, there were three peaks in the number of reported cases of
whooping cough. After 1981, the number of cases of whooping cough in each peak
decreased.
Use the information from the graph to suggest why.

A
  1. Vaccination rate increases;
  2. Fewer people to spread the disease / whooping cough / more people immune / fewer susceptible.
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16
Q

The percentage of the population vaccinated does not need to be 100% to be
effective in preventing the spread of whooping cough.
Suggest why.

A
  1. More people are immune / fewer people carry the pathogen;
  2. So susceptible / unvaccinated people less likely to contact infected
    people.
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17
Q

(a) Give two ways in which pathogens can cause disease.

A
  1. (Releases) toxins;
  2. Kills cells / tissues.
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18
Q

(b) Putting bee honey on a cut kills bacteria. Honey contains a high concentration of
sugar.
Use your knowledge of water potential to suggest how putting honey on a cut kills
bacteria.

A
  1. Water potential in (bacterial) cells higher (than in honey) / water

potential in honey lower (than in bacterial cells);

  1. Water leaves bacteria / cells by osmosis;
  2. (Loss of water) stops (metabolic) reactions.
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19
Q

Describe how HIV is replicated.

A
  1. Attachment proteins attach to receptors on helper T cell/lymphocyte;
  2. Nucleic acid/RNA enters cell;
  3. Reverse transcriptase converts RNA to DNA;
  4. Viral protein/capsid/enzymes produced;
  5. Virus (particles) assembled and released (from cell);
20
Q

Use your knowledge of phagocytosis to describe how an ADC enters and
kills the tumour cell.

A
  1. Cell ingests/engulfs the antibody/ADC
  2. Lysosomes fuse with vesicle/phagosome (containing ADC);
  3. Lysozymes breakdown/digest the antibody/ADC to release the drug;
21
Q

(b) Some of the antigens found on the surface of tumour cells are also found
on the surface of healthy human cells.
Use this information to explain why treatment with an ADC often causes
side effects.

A
  1. ADC will bind to non-tumour/healthy cells;
  2. Cause death/damage of non-tumour/healthy cells
22
Q

Suggest and explain two further investigations that should be done before
this ADC is tested on human breast cancer patients.

A
  1. Tested on other mammals to check for safety/side effects;
  2. Tested on (healthy) humans to check for safety/side effects;
23
Q

Describe how the human immunodeficiency virus (HIV) is replicated once inside helper T cells (TH cells).

A
  1. RNA converted into DNA using reverse transcriptase;
  2. DNA incorporated/inserted into (helper T cell)
    DNA/chromosome/genome/nucleus;
  3. DNA transcribed into (HIV m)RNA;
  4. (HIV mRNA) translated into (new) HIV/viral proteins (for assembly into viral particles);
24
Q

Use the information given to evaluate the use of BSCT to treat HIV infections.

A

For
1. (There appears to be) no virus/ HIV(-1)/RNA/DNA, so could be a cure/effective;
2. No CCR5/receptor, so not get HIV(-1) in the future 3. Only one transplant/BSCT needed (shown by patient Q)

Against
1. Don’t know if chemotherapy/radiotherapy is needed
2. Do not know if BSCT alone would be effective;
Do not know which ones having an effect.
3.Could be due to chemotherapy/radiotherapy;

25
Describe how a phagocyte destroys a pathogen present in the blood.
1. Engulfs 2. Forming vesicle/phagosome and fuses with lysosome 3. Enzymes digest/hydrolyse
26
Give two types of cell, other than pathogens, that can stimulate an immune response.
1. (Cells from) other organisms/transplants 2. Abnormal/cancer/tumour (cells) 3. (Cells) infected by virus
27
What is the role of the disulfide bridge in forming the quaternary structure of an antibody?
Joins two (different) polypeptides;
28
Explain how HIV affects the production of antibodies when AIDS develops in a person.
1. Less/no antibody produced; 2. (Because HIV) destroys helper T cells; 3. (So) few/no B cells activated / stimulated
29
Use all of this information to evaluate the effectiveness of the drug in treating AIDS.
Not effective in treating AIDS because 1. Number of T cells < 200 at 4 months; 2. (So) drug is not effective 3. Does not remove (all) HIV (particles) Effective in treating AIDS because Number of T cells > 200 after 5 months So drug is effective AIDS symptoms relieved/removed;
30
In Europe, viruses have infected a large number of frogs of different species. The viruses are closely related and all belong to the Ranavirus group. Previously, the viruses infected only one species of frog. (a) Suggest and explain how the viruses became able to infect other species of frog.
1. Mutation in the viral DNA/RNA/genome/genetic material; 2. Altered (tertiary structure of the) viral attachment protein; 3. Allows it/attachment protein/virus to bind (to receptors of other species);
31
Determining the genome of the viruses could allow scientists to develop a vaccine.
(The scientists) could identify proteins (that derive from the genetic code) (They) could (then) identify potential antigens (to use in the vaccine);
32
Describe how the B lymphocytes of a frog would respond to vaccination against Ranavirus. You can assume that the B lymphocytes of a frog respond in the same way as B lymphocytes of a human.
1. B cell (antibody) binds to (viral) specific/complementary receptor/antigen; 2. B cell clones 3. Plasma cells release/produce (monoclonal) antibodies (against the virus); 4. (B/plasma cells produce/develop) memory cells;
33
What is a monoclonal antibody?
(Antibodies with the) same tertiary structure
34
After a disease is diagnosed, monoclonal antibodies are used in some medical treatments. Give one example of using monoclonal antibodies in a medical treatment.
carries drug to specific cells/antigens/receptors
35
Describe the role of antibodies in producing a positive result in an ELISA test.
1. (First) antibody binds/attaches /complementary (in shape) to antigen; 2. (Second) antibody with enzyme attached is added; 3. (Second) antibody attaches to antigen; 4. (Substrate/solution added) and colour changes;
36
Describe and explain the role of antibodies in stimulating phagocytosis. Do not include details about the process of phagocytosis.
1. Bind to antigen 2. (Antibodies) cause clumping/agglutination
37
When a person is bitten by a venomous snake, the snake injects a toxin into the person. Antivenom is injected as treatment. Antivenom contains antibodies against the snake toxin. This treatment is an example of passive immunity. Explain how the treatment with antivenom works and why it is essential to use passive immunity, rather than active immunity.
1. (Antivenom/Passive immunity) antibodies bind to the toxin/venom/antigen and (causes) its destruction; 2. Active immunity would be too slow/slower;
38
Describe how phagocytosis of a virus leads to presentation of its antigens.
1. Phagosome / vesicle fuses with lysosome; 2. (Virus) destroyed by lysozymes / hydrolytic enzymes; 3. Peptides / antigen (from virus) are displayed on the cell membrane;
39
Describe how presentation of a virus antigen leads to the secretion of an antibody against this virus antigen.
1. Helper T cell / TH cell binds to the antigen (on the antigen- presenting cell / phagocyte); 2. This helper T / TH cell stimulates a specific B cell; 3. B cell clones
40
Collagen is a protein produced by cells in joints, such as the knee. Rheumatoid arthritis (RA) is an auto-immune disease. In an auto-immune disease, a person’s immune system attacks their own cells. RA causes pain, swelling and stiffness in the joints. Scientists have found a virus that produces a protein very similar to human collagen. Suggest how the immune response to this viral protein can result in the development of RA.
1. The antibody against virus (antigen) will bind to collagen; 2. This results in the destruction of the (human) cells / collagen;
41
What is an antigen?
1. Foreign protein 2. (that) stimulates an immune response / production of antibody;
42
What is an antibody?
1. A protein / immunoglobulin specific to an antigen; 2. Produced by B cells
43
Bacterial meningitis is a potentially fatal disease affecting the membranes around the brain. Neisseria meningitidis (Nm) is a leading cause of bacterial meningitis. (a) In the UK, children are vaccinated against this disease. Describe how vaccination can lead to protection against bacterial meningitis.
1. Antigen / epitope on surface of N. meninigitidis / bacterium binds to surface protein / surface receptor on a (specific single) B cell. 2. (Activated) B cell divides by mitosis / produces clone; 3. (Division) stimulated by cytokines / by T cells; 4. B cells / plasma cells release antibodies; 5. (Some) B cells become memory cells; 6. Memory cells produce plasma / antibodies faster
44
When a vaccine is given to a person, it leads to the production of antibodies against a disease-causing organism. Describe how.
1. Vaccine contains antigen from pathogen; 2. Macrophage presents antigen on its surface; 3. T cell with complementary receptor protein binds to antigen; 4. T cell stimulates B cell; 5. (With) complementary antibody on its surface; 6. B cell secretes large amounts of antibody; 7. B cell divides to form clone all secreting /producing same antibody.
45
Describe the difference between active and passive immunity.
1. Active involves memory cells, passive does not; 2. Active involves production of antibody by plasma cells /memory cells; 3. Passive involves antibody introduced into body from outside /named source; 4. Active long term, because antibody produced in response toantigen; 5. Passive short term, because antibody (given) is broken down; 6. Active (can) take time to develop / work, passive fast acting.