biology-the immune response Flashcards

1
Q

Describe how HIV is replicated.
4 marker

A

(1)- attachment proteins attach to receptors on the helper t cells
(1)-RNA enters cell
(1)-reverse transcriptase converts RNA to DNA
(1)- viral proteins are produces and viral particles are assembled and released from the cell

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2
Q

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

A

(1)- cell engulfs ADC
(1)- lysosome fuses with vesicle
(1)-lysozymes enzymes digest ADC to release drug

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3
Q

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.
2 marker

A

(1)- ADC will bind to healthy cells
(1)- causing damage to healthy cells

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4
Q

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

A

(1)- test different concentrations of ADC to find safe dosage
(1)- test on other mammals to check for side effects

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5
Q

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

A

(1)- reverse transcriptase coverts DNA to RNA
(1)-DNA is injected into helper T cell
(1)- DNA is transcribed into HIV mRNA
(1)- HIV mRNA is translated into new viral proteins

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6
Q

HIV-1 is the most common type of HIV. HIV-1 binds to a receptor on TH cells called CCR5.
Current treatment for HIV-1 involves the use of daily antiretroviral therapy (ART)
to stop the virus being replicated. Only 59% of HIV-positive individuals have access to ART.
Scientists have found that two HIV-1-positive patients (P and Q) have gone into remission (have no detectable HIV-1). This happened after a blood stem cell transplant (BSCT).
* Patient P was given two BSCTs, and patient Q was given one BSCT.
* All BSCTs came from a donor with TH cells without the CCR5 receptor.
* In addition, patient P had radiotherapy, and patient Q had chemotherapy.
Both of these treatments are toxic.
* Both patients (P and Q) stopped receiving ART 16 months after BSCT.
18 months after stopping ART, both patients had no HIV-1 RNA in their plasma,
no HIV-1 DNA in their TH cells and no CCR5 on their TH cells.
(b) Use the information given to evaluate the use of BSCT to treat HIV infections
5 marker

A

for
(1)- no virus so could be effective
(1)- do not have to take daily
(1)- no CCR5, so nothing for HIV-1 to bind to

against
(1)- only worked in 2 cases
(1)-do not which treatment is having the effect
(1)- might not be long term/18 months
(1)-do not know if chemotherapy or radiotherapy would be needed

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7
Q

Describe how a phagocyte destroys a pathogen present in the blood.
3 marker

A

(1)-phagocyte engulfs the pathogen through endocytosis and forms a phagosome
(1)-lysosome fuses with phagosome
(1)-lysozymes digest pathogen

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8
Q

What is the role of the disulfide bridge in forming the quaternary structure of an antibody?
1 marker

A

joins two polypeptides

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9
Q

Explain how HIV affects the production of antibodies when AIDS develops in a person.
3 marker

A

(1)- no antibodies are produced
(1)- due to HIV destroying helper t cells
(1)- so no B cells can be activated to undergo mitosis and form plasma cells

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10
Q

Use all of this information to evaluate the effectiveness of the drug in treating AIDS.
5 marker

A

not effective
(1)- number of HIV particles is constant
(1)-unknown side effects
(1)- only one person was used
(1)- number of T cells is under 200 at 4 months so not effective
effective
(1)-number of T cells was over 200 at 5 months os shows its effective. AIDS symptoms have been relieved

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11
Q

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 Suggest and explain how the viruses became able to infect other species of frog
2 marker

A

(1)- mutation in viral RNA
(1)- altered viral attachment protein
(1)- allows attachment proteins to bind to receptors of other species

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12
Q

Determining the genome of the viruses could allow scientists to develop a
vaccine.
Explain how.
2 marker

A

(1)- scientists could identify the proteome
(1)- they could then identify potential antigens to use in the vaccine

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13
Q

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.
Do not include details of the cellular response in your answer.
3 marks

A

(1)- b cell antibody binds to viral complementary antigen
(1)- b cell divided by mitosis
(1)- palm cell produce antibodies and produce memory cells

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14
Q

What is a monoclonal antibody?
1 marker

A

antibodies with the same tertiary structure produced from identical plasma cells

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15
Q

Describe the role of antibodies in producing a positive result in an ELISA test.
4 marker

A

(1)-(First) antibody binds/attaches /complementary (in shape) to antigen;
(1)-(Second) antibody with enzyme attached is added;
(1)- (Second) antibody attaches to antigen;
(1)-(substrate added and colour changes;

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16
Q

Describe and explain the role of antibodies in stimulating phagocytosis.
Do not include details about the process of phagocytosis.
2 marker

A

(1)-bind to antigen
(1)- antibodies cause agglutination which attract phagocytes

17
Q

When a vaccine is given to a person, it leads to the production of
antibodies against a disease-causing organism. Describe how.
5 marker

A
  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.
18
Q

Describe the difference between active and passive immunity.
5 marker

A
  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 to
    antigen;
  5. Passive short term, because antibody (given) is broken down;
  6. Active (can) take time to develop / work, passive fast acting.
19
Q

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.
6 marker

A
  1. Antigen binds to surface protein 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
20
Q

question 8-12