2.4- cell recognition and immune system Flashcards

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1
Q

7 box . 1 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.
[2 marks]

A
  1. (Antivenom/Passive immunity) antibodies
    bind to the toxin/venom/antigen and
    (causes) its destruction;
  2. Active immunity would be too slow/slower;
1. For ‘bind’ accept ‘attach’,
ignore ‘attack’.
1. For ‘destruction of toxin’
accept agglutination or
phagocytosis.
1. Ignore reference to
antibodies ‘neutralising
toxin/stopping damage’
1. Reject reference to
‘killing’ toxin/venom.
2. Accept ‘passive immunity
is faster’, not simply
‘passive immunity is fast’.

This question was all based on section 3.2.4 of the specification, in the novel context of production
of snake antivenom.
There were two parts to question 07.1 – how does an antibody work and what is the difference
between passive and active immunity? 28.1% of students could answer both of these correctly.
Confusion was demonstrated between antigens on a toxin and antibody binding to a pathogen.
Errors resulting in the first marking point not being awarded included describing binding, but failing
to discuss destruction, or discussing destruction without reference to binding. Commonly, students
used the idea of ‘complementary’ in place of binding. Those who were not awarded marking point
two tended not to make a comparative statement about active and passive immunity, and some
made vague statements about active immunity ‘taking time’, rather than expressing length of time.
A mark of zero was commonly the result of confusing active and passive immunity or treating the
antivenom as a vaccine which would then trigger an immune response.

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2
Q

Figure 8 shows a procedure used to produce antivenom. box
Figure 8

7 . 2 A mixture of venoms from several snakes of the same species is used.
Suggest why.
[2 marks]

A
. May be different form of antigen/toxin
(within one species)
OR
Snakes (within one species) may have
different mutations/alleles;
2. Different antibodies (needed in the
antivenom)
OR
(Several) antibodies complementary (to
several antigens);

In 07.2, many students gave answers relating to not needing to identify the species of snake that
had bitten a person, as the antivenom would work against the venom of several species – this was
not creditworthy as the question is clearly related to several snakes of the same species. A pleasing number of students understood the production of antivenom and appreciated the need for
several antibodies to be produced by the animal to be used in the patient. Some suggested that
one antibody could be effective against several antigens; this was not given credit. Pleasingly, few
students confused antigens and antibodies. Common errors included referring to different forms of
venom, which was indicated in the question stem, or failing to include reference to antibodies and
instead making vague statements about “being effective against” or “fighting off” or
“neutralising/counteracting” the venom. Roughly even proportions of students scored two, one and
zero marks for this question

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3
Q

0 7 box . 3 Horses or rabbits can be used to produce antivenoms.
When taking blood to extract antibody, 13 cm3 of blood is collected per kg of the
animal’s body mass.
The mean mass of the horses used is 350 kg and the mean mass of the rabbits used
is 2 kg
Using only this information, suggest which animal would be better for the production of
antivenoms.
Use a calculation to support your answer.
[2 marks]

A
  1. Horses because more
    antivenom/antibodies could be collected
    (as more blood collected);
2. 4550 (cm3
) v 26 (cm3
) (blood collected)
2. Accept 175 rabbits
needed to (collect the
volume of blood from) one
horse.

In question 07.3, most students could complete the required calculation. Even so, many students
suggested the rabbit would be better as it would likely be safer for the rabbit as less blood was
removed or suggested that the same number of antibodies would be produced in a smaller volume
of blood. Of those who did pick the horse, many only stated that more blood could be collected,
rather than linking this to more antibodies/antivenom being collected from each animal. 81% of
students scored at least one mark here.

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4
Q

0 7 . 4 During the procedure shown in Figure 8 the animals are under ongoing observation
by a vet.
Suggest one reason why [1 mark]

A
  1. (So) the animal does not suffer from the
    venom/vaccine/toxin;
  2. (So) the animal does not suffer
    anaemia/does not suffer as a result of
    blood collection;
  3. (So) the animal does not have pathogen
    that could be transferred to humans;

Too many generalised answers were given to question 07.4. At this level, a specific reason why it
would be ethical to have veterinary supervision in this particular procedure was required.
Confusion was sometimes demonstrated here over whether the animals were being administered
venom or antivenom.

Accept ‘To fulfil
licence/legal requirements’.
Accept ‘(So) the animal
does not have pathogen
that could result in it
producing other antibodies
(not wanted in the
antivenom)’.
For ‘pathogen’ accept
correct form of pathogen.
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5
Q

7 box . 5 During vaccination, each animal is initially injected with a small volume of venom.
Two weeks later, it is injected with a larger volume of venom.
Use your knowledge of the humoral immune response to explain this vaccination
programme.
[3 marks]

A
  1. B cells specific to the venom reproduce by
    mitosis;
  2. (B cells produce) plasma cells and memory
    cells;
  3. The second dose produces antibodies (in
    secondary immune response) in higher
    concentration and quickly
    OR
    The first dose must be small so the animal
    is not killed;
1. Accept in context of
primary or secondary
immune response.
1. Credit idea of specificity if
given once in relation to T
or B cell.
1. Accept a description for
specificity.
1. Accept ‘clone’ for
‘reproduce by mitosis’.
1. ‘Clonal selection of B
cells’ = MP1.
3. Accept ‘a lot of antibody’
for ‘higher concentration of
antibody

In 07.5, very few students could give a complete account of the humoral immune response in this
context, but those who could (7.3%) gave some excellent answers. It was rare to see the idea of
specificity to the venom antigens being key to the B-cells cloning, and confusion was demonstrated
between T-cells and B-cells and which produced antibodies. About half of the students achieved
the second marking point for recognising the two differentiated forms of B-cells, but beyond this
many did not achieve any further marks due to vague statements or misconceptions. A small
number of students demonstrated a more detailed understanding but still did not obtain marks due
to key ideas being missed. Examples included the idea of specificity of T/B-cells missing from their
answer for marking point 1, mitosis/cloning missing from marking point 2, or one of the ideas of
high concentration or ‘quickly’ missing from marking point 3.

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6
Q

0 7 . 1 Describe how phagocytosis of a virus leads to presentation of its antigens.
[3 marks]

A
  1. Phagosome/vesicle fuses with lysosome;
  2. (Virus) destroyed by lysozymes/hydrolytic
    enzymes;
  3. Peptides/antigen (from virus) are displayed on
    the cell membrane;
  4. Accept vacuole
    fuses with lysosome
  5. Reject virus fuses
    with lysosome

07.1 Many students did not refer to the antigen being presented on the surface membrane of the
phagocyte, so could not be awarded mark point 3.

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7
Q

0 7 . 2 Describe how presentation of a virus antigen leads to the secretion of an antibody
against this virus antigen.
[3 marks]

A
  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
    OR
    B cell divides by mitosis;
  4. (Forms) plasma cells that release antibodies;

07.2 Some students described, once again, how the virus would be presented. Mark points 3
and 4 were more often awarded than mark points 1 and 2, suggesting better understanding
of the actions of B cells in the immune response than T cell involvement. Mark point 1

ould be awarded if the student stated that a T cell binds to the antigen and then
differentiates into a T helper cell.

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8
Q

0 7 . 3 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.
[2 marks]

A
  1. The antibody against virus (antigen) will bind
    to collagen;
  2. This results in the destruction of the (human)
    cells/collagen;

07.3 The responses to this question revealed much misunderstanding of the immune response
as a whole, with many references to ‘thinking’ immune systems. Many students simply
repeated phrases from the question stem; for example, “since the virus protein and the
human collagen have a similar shape, the immune system will attack the human collagen”.
Students needed to identify that the part of the immune response which would ‘attack’ the
collagen would be the binding of specific antibodies, and then to use their knowledge of
how an antigen-antibody complex leads to the destruction of the antigen (section 3.2.4 of
the specification), i.e., human collagen in this case. Credit could be gained for reference to
agglutination or phagocytosis as methods of ‘attacking’ the human collagen, since these
are the methods of antigen destruction named in the specification.

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9
Q

0 1 . 2 When HIV infects a human cell, the following events occur.
• A single-stranded length of HIV DNA is made.
• The human cell then makes a complementary strand to the HIV DNA.
The complementary strand is made in the same way as a new complementary
strand is made during semi-conservative replication of human DNA.
Describe how the complementary strand of HIV DNA is made.
[3 marks]

A
  1. (Complementary) nucleotides/bases pair
    OR
    A to T and C to G;
  2. DNA polymerase;
  3. Nucleotides join together (to form new
    strand)/phosphodiester bonds form;
  4. & 3. Ignore ‘(DNA
    polymerase) forms
    base pairs/nucleotide
    pairs’
    If clearly writing rote
    answer about DNA
    replication 2 max e.g.
    helicase or separating
    strands

Question 1.2 discriminated very well, with 15% obtaining three marks and 21% scoring zero.
There were good, concise answers that scored three marks for including complementary base
pairing and the role of DNA polymerase in joining nucleotides together to form the new DNA
strand; often in two or three lines.
Many students failed to read the question carefully and did not answer the question as set. They
wrote at length about DNA replication, starting with DNA helicase. These answers were awarded a
maximum of two marks, because the question specifically asked how the complementary strand of
HIV DNA is made. Many students appeared to believe that DNA actively pulls free nucleotides into
place and makes them base pair; some even wrote about condensation reactions. There were
students who confused transcription with replication and gave accounts of mRNA production.
Some students appeared to focus on ‘HIV’ and ‘replication’ and gave an extended account of how
HIV infects cells, uses reverse transcriptase to make DNA, incorporates its DNA into host DNA,
takes over the cell, is replicated by the host cell, infects new cells and leads to AIDS. They often
went onto an additional page, or wrote their answer under 1.3 on the next page, in breach of
instructions given on the front of the exam pap

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10
Q

0 1 . 3 Contrast the structures of DNA and mRNA molecules to give three differences.
[3 marks]

A
1. DNA double stranded/double helix and
mRNA single-stranded;
2. DNA (very) long and RNA short;
3. Thymine/T in DNA and uracil/U in RNA;
4. Deoxyribose in DNA and ribose in RNA;
5. DNA has base pairing and mRNA doesn’t/
DNA has hydrogen bonding and mRNA
doesn’t;
6. DNA has introns/non-coding sequences
and mRNA doesn’t;

In 1.3, it was pleasing to find that many students did obey the command word to ‘contrast’ and
gave full statements about the differences between DNA and RNA. Many students knew enough
about the structures of DNA and mRNA to give correct contrasting features and 47% obtained all
three marks.

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11
Q

0 7 . 1 Human papilloma virus (HPV) is the main cause of cervical cancer. A vaccine
has been developed to protect girls and women from HPV.
Describe how giving this vaccine leads to production of antibody against HPV.
[4 marks]

A
1. Vaccine/it contains antigen (from
HPV);
2. Displayed on antigen-presenting cells;
3. Specific helper T cell (detects antigen
and) stimulates specific B cell;
4. B cell divides/goes through
mitosis/forms clone to give plasma
cells;
5. B cell/plasma cell produces antibody;

7.1 was a very good discriminator. 19% obtained all four marks, 14% failed to score and equal
percentages obtained one, two or three marks. Many students had the idea that a vaccine contains
antigen and knowledge of antigen-presenting cells was common. There were also many correct
statements about plasma/B cells releasing antibodies. Fewer students had the idea of a B cell
dividing to form plasma cells. Not many students were able to express clearly the idea of a specific
helper T cell or B cell detecting, or responding to, a specific antigen. Quite a few students got
confused between the roles of T cells and B cells. Some students wrote at length about memory
cells and secondary responses, neither of which was required to answer the question. As in some
other questions, this inclusion of irrelevant material often generated additional pages and wasted
time that could have been spent on other questions.

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12
Q
Figure 5 shows a test that has been developed to find out if a person has antibodies
to the human immunodeficiency virus (HIV) antigen.
Figure 5
This test only detects the presence of HIV antibodies. Give two reasons why it cannot
be used to find out if a person has AIDS.
 [2 marks]
0 7 . 1
HIV antigens are attached to
a test well in a dish.
A sample of blood plasma is
added to the well.
If HIV antibodies are present,
they bind to the HIV antigen.
The well is washed.
A second antibody with an
enzyme attached is then
added.
This binds specifically to the
HIV antibody.
The well is washed again.
A yellow solution is added,
which changes to blue if the
enzyme is present. A blue
colour shows that the person
has HIV antibodies.
Step 1
Step 2
Step 3
Step 4
7

This test only detects the presence of HIV antibodies. Give two reasons why it cannot
be used to find out if a person has AIDS.
[2 marks]

A

(To diagnose AIDS, need to look for/at)

  1. (AIDS-related) symptoms;
  2. Number of helper T cells;
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13
Q

he solution will remain yellow if a person is not infected with HIV. Explain why.
[2 marks]

A
  1. HIV antibody is not present;
  2. (So) second antibody/enzyme will not bind/is
    not present;
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14
Q

A mother who was infected with HIV gave birth to a baby. The baby tested positive
using this test. This does not prove the baby is infected with HIV.
Explain why.
[2 marks]

A
  1. Children receive (HIV) antibodies from their
    mothers/maternal antibodies;
  2. (So) solution will always turn blue/will always
    test positive (before 18 months)
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15
Q

A control well is set up every time this test is used. This is treated in exactly the same
way as the test wells, except that blood plasma is replaced by a salt solution.
Use information from Figure 5 to suggest two purposes of the control well.
[2 marks]

A

(Shows that)
1. Only the enzyme/nothing else is causing a
colour change;
2. Washing is effective/all unbound antibody is
washed away;

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16
Q

Q1.(a) Give two ways in which pathogens can cause disease. (2)

A
  1. (Releases) toxins;
  2. Kills cells / tissues.
  3. Accept any reference to cell / tissue damage
    Ignore infecting / invading cells
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17
Q

Q2.Whooping cough is a disease that affects some infants. Doctors collected data relating to
whooping cough between 1965 and 1996.
They collected data for:
• the number of cases of whooping cough reported
• the percentage of infants vaccinated against whooping cough.

(a) Suggest two reasons why the percentage of infants vaccinated decreased between
1973 and 1975. (2)

A

Any two from:

  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.
  4. Too expensive unqualified is insufficient for mark
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18
Q

(b) 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 (2)

A

(b) 1. Vaccination rate increases;
2. Fewer people to spread the disease / whooping cough / more people
immune / fewer susceptible.
2. Neutral − greater herd effect
2. Allow description of immune
Q Reject ‘resistant’.

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19
Q

(c) The percentage of the population vaccinated does not need to be 100% to be
effective in preventing the spread of whooping cough.
Suggest why. (2)

A
  1. More people are immune / fewer people carry the pathogen;
    If neither point 1 or 2 awarded
    Herd immunity = 1 mark
  2. So susceptible / unvaccinated people less likely to contact infected
    people.
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20
Q

Q4.(a) (i) A mutation of a tumour suppressor gene can result in the formation of a tumour.
Explain how. (2)

A

) 1. (Tumour suppressor) gene inactivated / not able to control / slow down
cell division;
Ignore: references to growth

  1. Rate of cell division too fast / out of control.
    1 and 2 Accept: mitosis
    1 and 2 Reject: meiosis
21
Q

(ii) Not all mutations result in a change to the amino acid sequence of the
encoded polypeptide.
Explain why.
…………………….. (1)

A
(ii) 1. (Genetic) code degenerate;
Accept: codon for triplet
Accept description of degenerate code, e.g. another triplet
codes for the same amino acid
2. Mutation in intron.
Accept: mutation in non-coding DNA
22
Q

(b) 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. (3)

A

) 1. Antibody has specific tertiary structure / binding site / variable region;
Do not accept explanations involving undefined antigen

  1. Complementary (shape / fit) to receptor protein / GF / binds to receptor
    protein / to GF;
    Ignore: same shape as receptor protein / GF
  2. Prevents GF binding (to receptor)
23
Q

Q5.Read the following passage.

Herpes simplex virus (HSV) infects nerve cells in the face, including some near the
lips. Like many other viruses, HSV can remain inactive inside the body for years.
When HSV becomes active, it causes cold sores around the mouth.
Human cells infected with a virus may undergo programmed cell death. While HSV
is inactive inside the body, only one of its genes is transcribed. This gene is the
latency-associated transcript (LAT) gene that prevents programmed cell death of an
infected nerve cell.
5
Scientists have found that transcription of the LAT gene produces a microRNA.
This microRNA binds to some of the nerve cell’s own mRNA molecules. These
mRNA molecules are involved in programmed cell death of nerve cells. The
scientists concluded that production of this microRNA allows HSV to remain in the
body for years.
10
Use information from the passage and your own knowledge to answer the following
questions.
(a) HSV infects nerve cells in the face (line 1). Explain why it infects only nerve cells.

(3)

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.
    Accept converse argument
24
Q

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

A

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

25
Q

(c) Suggest one advantage of programmed cell death (line 4).
(1)

A

) Prevents replication of virus.

26
Q

(d) 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. (4)

A

MicroRNA binds to cell’s mRNA (no mark)

  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.
27
Q

Q6.Malaria is a disease caused by parasites belonging to the genus Plasmodium. Two species
that cause malaria are Plasmodium falciparum and Plasmodium vivax.
A test strip that uses monoclonal antibodies can be used to determine whether a person is
infected by Plasmodium. It can also be used to find which species of Plasmodium they are
infected by.
• A sample of a person’s blood is mixed with a solution containing an antibody, A, that
binds to a protein found in both species of Plasmodium. This antibody has a
coloured dye attached.
• A test strip is then put into the mixture. The mixture moves up the test strip by
capillary action to an absorbent pad.
• Three other antibodies, B, C and D are attached to the test strip. The position of
these antibodies and what they bind to is shown in Figure 1.

(a) Explain why antibody A attaches only to the protein found in species of
Plasmodium. (1)

A
  1. Antibody has tertiary structure;

2. Complementary to binding site on protein.

28
Q

(b) Antibody B is important if this test shows a person is not infected with Plasmodium.
Explain why antibody B is important. (2)

A
  1. Prevents false negative results;
  2. (Since) shows antibody A has moved up strip / has not bound to any
    Plasmodium protein.
29
Q

(c) One of these test strips was used to test a sample from a person thought to be
infected with Plasmodium. Figure 2 shows the result.
Figure 2

What can you conclude from this result?
Explain how you reached your conclusion. (4)

A
  1. Person is infected with Plasmodium / has malaria;
  2. Infected with (Plasmodium) vivax;
  3. Coloured dye where antibody C present;
  4. That only binds to protein from vivax / no reaction with antibody for
    falciparum.
    Person is infected with P. vivax / Plasmodium vivax = 2
    marks (MP1 and MP2)
30
Q

A potential new cancer treatment involves what are known as magic bullets. Cancer cells have
cell-surface antigens which are not found on normal cells. Antibodies are produced to one of
these antigens by the monoclonal antibody technique. Once the antibody molecules have been
made, an enzyme is attached to them and the antibody-enzyme complex is injected into the
patient. A drug, which causes cell lysis, is then injected in an inactive form. Use the information in the passage to suggest how the drug kills only cancer cells. 3 MARKS

A

Antibody binds/eq/recognises only to cancer cells;
because of antibody-antigen binding/eg;
enzyme activates the drug;
at cancer cells only;

31
Q

Explain the role of B-lymphocytes and T-lymphocytes in the defence of the body against
a virus infection. 6 MARKS

A

B lymphocytes produce antibodies/involved in humoral response;

T lymphocytes involved in cell mediated immunity;

Macrophages present antigens;

(specific) B lymphocytes recognise/bind to antigen;

increase in numbers by mitosis;

produce plasma cells (which make antibodies);

killer T cells kill virus infected cells;

32
Q

Immunisation programmes may use either attenuated or dead microorganisms. Suggest
why there might be problems for the patient when using these vaccines. 3 MARKS

A

Process of killing organisms might not be 100% efficient;
live organisms might give rise to full-blown disease;
named side effects, eg allergies

33
Q

The diagram shows one way in which white blood cells protect the body against disease
Describe what is happening during Stage 1. 2 MARKS

A

Formation of vesicle / phagocytosis;

Derived from plasma membrane

34
Q

Describe the role of Organelle A in the defence against disease. TWO MARKS

A

Contain hydrolytic enzymes;

To break down / digest bacterium

35
Q

What is an attenuated microorganism? ONE MARK

A

Weakened organism;

36
Q

Describe how memory cells protect the body from disease. 3 MARKS

A

On further exposure to same microorganism;
Antigen recognised;
Faster response;
Greater production of antibodies;

37
Q

What is an antigen? ONE MARK

A

A molecule which stimulates an immune response / antibody
production / surface protein / glycoprotein / non-self protein;

Explain the importance of cell type Y in immunity.2 MARKS
Carried (an i

38
Q

Explain the importance of cell type Y(memory ) in immunity.2 MARKS

A

Carried (an immunological) memory of the specific antigen;

Rapid production of antibodies;

39
Q

Influenza and measles are diseases caused by viruses. The viruses have antigens on their
surface. Use your knowledge of antigens and antibodies to suggest why a person may
have influenza several times, but usually has measles only once. 3 MARKS

A
Measles: One antigen/
unchanging One type of memory
cell/ antibody
needed
Influenza: Several antigens/
changing Several types of
memory cell/
antibodies needed;
40
Q

Myeloid leukaemia is a type of cancer. Monoclonal antibodies are used in treating
it. A monoclonal antibody will bind to an antigen on a myeloid leukaemia cell. It
will not bind to other types of cell. Explain why this antibody binds only to an
antigen on a myeloid leukaemia cell.
………………………………………………………………. 2 MARKS

A

These antigens/antibodies have complementary/particular shape;
Allow fitting/binding with (relevant) antibody/antigen;

41
Q

Calichaemicin is a substance which is very toxic and kills cells. Scientists have made a
drug by joining calichaemicin to the monoclonal antibody that attaches to myeloid
leukaemia cells. Explain why this drug is effective in treating myeloid leukaemia. 2 MARKS

A

Calichaemicin delivered specifically to cancer cells/less likely to/will
not harm normal/healthy cells;
Lower dose of calichaemicin needed to be effective;

42
Q

Although this vaccine is made from antigens from malarial parasites, it does not
cause malaria. Explain why this vaccine does not cause malaria.

A

antigens are only single molecules/part of parasite;

do not actually cause disease;

43
Q

Vaccines protect people against disease. Explain how. 5 MARKS

A
  1. Vaccines contain antigens / antigens are injected;
  2. Dead pathogens / weakened pathogens;
  3. Memory cells made;
  4. On second exposure memory cells produce antibodies / become active / recognise pathogens;
  5. Rapidly produce antibodies / produces more antibodies;
44
Q

Describe the difference between active and passive immunity 5 MARKS

A

.1. Active involves memory cells, passive does not;

  1. Active involves production of antibody by plasma cells / memory cells;
  2. Active long term, because antibody produced in response to antigen;
  3. Passive short term, because antibody (given) is broken down;
  4. Active (can) take time to develop / work, passive fast acting;
45
Q

What is a monoclonal antibody? 2 MARKS

A

antibodies all the same / from one type of plasma cell;

specific to / complementary to / fits only one antigen;

46
Q

Phagocytes and lysosomes are involved in destroying microorganisms. Describe how. 4 MARKS

A

Phagocytes engulf pathogens/microorganisms;
Enclosed in a vacuole / vesicle/ phagosome;
Lysosomes have enzymes;
That digest/hydrolyse molecules/proteins/lipids/ microorganism;

47
Q

Describe how the MMR vaccine results in immunity 7 MARKS

A
1 Three different viruses (in vaccine);
2 With antigen (on each virus);
3 Different for each (virus);
4 Macrophage/phagocyte presents antigen;
5 Binds to/activates (receptor protein on) T-cells;
6 T-cells activate B-cell;
7 Antigen binds to antibody on B-cell;
48
Q

Describe how B-lymphocytes respond when they are stimulated by antigens.(4 marks)

A

divide by mitosis / form clones;
produce plasma cells;
(plasma cells) make antibodies;
(plasma cells) produce memory cells;

49
Q

Describe how new viruses are produced after HIV has infected a T cell. (4/6 marks)

A

(b) DNA copy made (of viral RNA);
Inserted into host DNA / chromosomes;
(Uses viral DNA to) make viral proteins/particles;
Makes viral RNA;
(Host) cell makes new viruses;
“Budding off” / wrapped in cell membrane;
Accept reverse transcriptase makes DNA for 2 marks in correct context;3 max