3.2.4 Cell recognition and the immune system

Question 1

Describe how HIV is replicated

Answer 1

1. attachment proteins attach to receptors on T helper cells
2. RNA enters TH cell
3. reverse transcriptase converts RNA to DNA - DNA incorporated into TH cell
4. viral protein/capsid/enzymes produced
5. virus particles are assembled and released from cell

Question 2

describe how HIV is replicated once inside T helper cells.

Answer 2

1. reverse transcriptase converts RNA to DNA
2. DNA transcribed into HIV m(RNA)
3. HIV mRNA translated into (new) HIV / viral proteins/ for assembly into viral particles

Question 3

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

Answer 3

HIV destroys T-Helper cells
T- Helper cells stimulate B cells
B cells produce antibodies so less antibodies would be produced.

Question 4

determining the genome of viruses can allow scientists to develop a vaccine
explain how

Answer 4

scientists could identify proteins from the genetic code
they could then identify potential antigens to use in the vaccine

Question 5

what is an antigen?

Answer 5

• cell-surface molecule which stimulate immune response
• usually (glyco)protein sometimes (glyco)lipid or polysaccharide
  -immune system recognises as “self” or “non-self” = enables identification of cells from other organisms of the same species, pathogens, toxins & abnormal body cells

Question 6

how does phagocytosis destroy pathogens?

Answer 6

1. phagocyte moves towards pathogen via chemotaxis
2. phagocyte engulfs pathogen via endocytosis to form a phagosome
3. phagosome fuses with lysosome (phagolysosome).
4. lysozymes digest pathogen
5. phagocyte absorbs the products from pathogen hydrolysis

Question 7

explain the role of antigen-presenting cells (APCs)

Answer 7

macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis)
enhances recognition by T-H cells, which cannot directly interface with pathogens/ antigens in body fluid

Question 8

give 2 differences between specific and nonspecific immune responses.

Answer 8

nonspecific (inflammation, phagocytosis) = same for all pathogens
specific (B & T lymphocytes) = complementary pathogen
nonspecific = immediate
specific = time lag

Question 9

name the 2 types of specific immune response

Answer 9

• cell-mediated
• humoral

Question 10

outline the process of the cell-mediated response

Answer 10

1. complementary T-H lymphocytes bind to foreign antigen on APC
2. release cytokines that stimulate:
   a) clonal expansion of complementary T-H cells (rapid mitosis): become memory cells or trigger humoral response
   b) clonal expansion of cytotoxic T cells (T-C): secrete enzyme perforin to destroy infected cells

Question 11

outline the process of the humoral response

Answer 11

1. complementary T-H lymphocytes bind to foreign antigen on antigen-presenting T cells
   2.release cytokines that stimulate clonal expansion (rapid mitosis) of complementary B lymphocytes
2. B cells differentiate into plasma cells
3. plasma cells secrete antibodies with complementary variable region to antigen

Question 12

what is an antibody?

Answer 12

proteins secreted by plasma cells
quaternary structure: 2 ‘light chains’ held together by disulfide bridges, 2 longer ‘heavy chains’
binding sites on variable region of light chains have specific tertiary structure complementary to an antigen
the rest of the molecule is known as the constant region

Question 13

how do antibodies lead to the destruction of a pathogen?

Answer 13

formation of antigen-antibody complex results in agglutination, which enhances phagocytosis

Question 14

what are monoclonal antibodies?

Answer 14

antibodies produced from a single clone of B cells

Question 15

what are memory cells?

Answer 15

• specialised T-H/ B cells produced from primary immune response
• remain in low levels in the blood
• can divide very rapidly by mitosis if organism encounters the same pathogen again.

Question 16

contrast the primary and secondary immune response.

Answer 16

secondary response:
- faster rate of antibody production
- shorter time lag between exposure & antibody production.
- higher concentration of antibodies
- antibody level remains higher after the secondary response
- pathogen usually destroyed before any symptoms

Question 17

what causes antigen variability?

Answer 17

1. Random genetic mutation changes DNA base sequence
2. Results in different sequence of codons on mRNA
3. Different primary structure of antigen = H-bonds, ionic bonds & disulfide bridges form in different places in tertiary structure
4. Different shape of antigen

Question 18

explain how antigen variability affects the incidence of disease.

Answer 18

• memory cells no longer complementary to antigen = individual not immune = can catch the disease more than once.
• many varieties of a pathogen = difficult to develop vaccine containing all antigen types.

Question 19

compare passive and active immunity. give examples of both types.

Answer 19

• both involve antibodies
• can both be natural or artificial
  passive natural: antibodies in breast milk/ across placenta
  passive artificial: anti-venom, needle stick injections
  active natural: humoral response to infection
  active artificial: vaccination

Question 20

what are the differences between passive and active immunity?

Answer 20

passive doesn’t involve memory cells and antibodies not replaced when broken down = short term whereas active involves memory cells being produced = long term
passive is immediate active creates a time lag
passive involves antibodies from external source whereas active involves lymphocytes which produce antibodies
passive means direct contact with antigen is not necessary whereas active means direct contact with antigen is necessary

Question 21

explain the principles of vaccination

Answer 21

1. Vaccine contains dead/ inactive form of a pathogen or antigen
2. Triggers primary immune response
3. Memory cells are produced and remain in the bloodstream, so secondary response is rapid & produces higher concentration of antibodies.
4. Pathogen is destroyed before it causes symptoms

Question 22

what is herd immunity?

Answer 22

vaccinating large proportion of population reduces available carriers of pathogen.
protects individuals who have not been vaccinated e.g. those with a weak immune system

Question 23

suggest some ethical issues surrounding the use of vaccines.

Answer 23

• production may involve use of animals
• potentially dangerous side-effects
• clinical tests may be fatal
• compulsory vs opt-out

Question 24

describe the structure of HIV

Answer 24

• genetic material (2xRNA) & viral enzymes (integrase & reverse transcriptase) surrounded by capsid
• surrounded by viral envelope derived from host cell membrane
• GP120 attachment proteins on surface

Question 25

how does HIV result in the symptoms of AIDS?

Answer 25

1. Attachment proteins bind to complementary CD4 receptor on T-H cells.
2. HIV particles replicate inside T-H cells, killing or damaging them.
3. AIDS develops when there are too few T-H cells for the immune system to function
4. Individuals cannot destroy other pathogens & suffer from secondary diseases/ infections.

Question 26

why are antibiotics ineffective against viruses?

Answer 26

Antibiotics often work by damaging murein cell walls to cause osmotic lysis. Viruses have no cell wall.
Viruses replicate inside host cells = difficult to destroy them without damaging normal body cells.

Question 27

suggest the clinical applications of monoclonal antibodies.

Answer 27

• pregnancy tests by detecting HCG hormones in urine
• diagnostic procedures e.g. ELISA test
• targeted treatment by attaching drug to antibody so that it only binds to cells with abnormal antigen e.g. cancer cells due to specificity of tertiary structure of binding site

Question 28

explain the principle of a direct ELISA test.

Answer 28

detects presence of specific antigen
1. Monoclonal antibodies bind to bottom of test plate
2. Antigen molecules in sample bind to antibody. Rinse excess
3. Mobile antibody with ‘reporter enzyme’ attached binds to antigens that are ‘fixed’ on the monoclonal antibodies. Rinse excess.
4. Add substrate for reporter enzyme. Positive result: colour change

Question 29

explain the principle of an indirect ELISA test.

Answer 29

detects presence of an antibody against a specific antigen
1. Antigens bind to bottom of test plate
2. Antibodies in sample bind to antigen. Wash away excess.
3. Secondary antibody with ‘reporter enzyme’ attached binds to primary antibodies from the sample
4. Add substrate for reporter enzyme. Positive result: colour change

Question 30

suggest some ethical issues surrounding the use of monoclonal antibodies

Answer 30

• production involves animals
• drug trials against arthritis & leukaemia resulted in multiple organ failure

Question 31

Why do Vaccines increase antibody concentration?

Answer 31

the vaccine contains the antigen
the antigen activates T-Helper cells
T-H cells stimulate B lymphocytes to delve lip into plasma cells
plasma cells produce antibodies

Question 32

why does antigen concentration increase more quickly when an individual is infected with a pathogen after they’ve been vaccinated?

Answer 32

Memory cells remain in the blood after the vaccination
The foreign antigens are recognised more quickly and less time is needed for lymphocytes with complementary receptors to be found

Question 33

why might people be concerned about vaccination?

Answer 33

harmful side effects
concerns around animal testing

Question 34

how do vaccines work?

Answer 34

• dead or weakened antigen injected
• stimulates T-H cells to release cytokines
• cytokines stimulate production of plasma cells
• B cells release antibodies
• Some b cells become memory cells
• memory cells produce antibodies faster