2.4 Cell recognition and the immune system Flashcards
1
Q
What other structures do some viruses have
A
Lipid envelope which is formed from the host cell membrane.
2
Q
What is it described as? What parts make up a virus?
What is a virus
A
A small, acellular structure (not a cell but a single particle) consisting of:
- A nucleic acid strand (RNA or DNA0
- Protein capsid made of units called capsomeres (coat)
- Attatchement proteins which help the virus penetrate host cells
3
Q
Is it general or specific? How do they differ?
What is a virus
A
- Specific to the type of cell it infects (e.g. the rabies virus only attacks brain or nervous cells).
- The specificity depends on the type of receptors found on the surface of the cell.
4
Q
How do viruses replicate
A
- Surface attatchment proteins bind to host cell.
- Nucleic acid is injected into the host cell which provides ‘instructions’ for host cells metabolic processes.
- The host cell then begins to produce viral components, nucleic acids, enzymes and structural proteins.
- These are then assembled into new viruses.
5
Q
Lysis - rupturing of cell
Describe the lytic cycle
A
- Virus attatches to host cell and injects its genetic material.
- Cell takes genetic material aand startes following the ‘instructions’.
- Causes the host cell to make more and more copies of the virus, causing the host cell membrane to rupture (lysis).
- This allows the viruses to leave the host cell and infect more cells in the body.
6
Q
Describe the lysogenic cycle
A
- Inject genetic material into bacteria cell.
- Genetic material stays hidden in host DNA.
- Means when host replicates, it also replicates the viral DNA.
- This can trigger the virus to go into the lytic cycle.
7
Q
What type of virus replicates via the lysogenic cycle
A
Usually bacteriophage virus - goes after bacteria.
8
Q
What is a pathogen (+ examples)
A
- Any infectious agent that causes disease or illness in a host.
- Can be: viruses, bacteria, fungi, protists or prions.
9
Q
How do pathogens cause disease in a host
A
- Damaging cells (e.g. bursting cells).
- Producing toxins and disrupting cell function.
10
Q
What are non-specific defence mechanisms + examples
A
- They produce an immediate response which is the same for all pathogens.
- E.g. Physical and chemical barriers, phagocytosis.
11
Q
What are examples of physical and chemical barriers
A
- Skin: a tough physical barrier consisting of keratin.
- Stomach acid: HCl which kills bacteria.
- Gut and skin flora: natural bacteria flora competes with pathogens for food and space.
12
Q
What is phagocytosis
A
- A process in which WBC engulf pathogens, destroying them.
- They do this by fusing to a pathogen and enclose them in a phagocytic vesicle with a lysosome.
- After the pathogen is engulfed and destroyed, its chemical markers (antigens) are presented on the surface of the phagocyte (now an antigen-presenting cell).
13
Q
Describe the process of phagocytosis
A
- Phagocyte is attracted to the pathogen by chemical products it produces.
- It moves towards the pathogen against a concentration gradient and several receptors bind to it.
- The phagocyte engulfs the pathogen, forming a phagosome-vesicle.
- Lysosomes inside the WBC move towards the vesicle and fuse with it, forming phagolysosomes.
- The lysosomes release their lysozymes (hydrolytic enzymes) into the phagosome where they hydrolyse the pathogen, destroying it.
- The soluble products are absorbed into the cytoplasm.
- The phagocyte presents the pathogen antigens on its own cell-surface membrane, forming an APC.
14
Q
What is an antigen
A
A foreign/ non-self protein that stimulates an immune response or the production of antibodies.
15
Q
Where are antigens found
A
- Pathogens
- Abnormal body cells (e.g. cancer cells)
- Non self material (e.g. cells from another human)
16
Q
What are specific defence mechanisms and what kind of cells do they involve
A
- The response is slower and specific to each pathogen.
- There are 2 types which both involve lymphocytes.
- The cell mediated response involves T-lymphocytes.
- The humoral response involves B-lymphocytes.
17
Q
Where are B cells found
A
They mature in the bone marrow.
18
Q
Where are T cells found
A
They move from the bone marrow to the thymus gland where they mature.
19
Q
What is the role of T cells and what are the 3 types
A
- They detect non-self/ foreign antigens.
- T cells interact with an APC which activates it (they collide and if complementary, they bind).
- 3 types: Helper T cells, Cytotoxic T cells and Memory T cells.
- All contain unique T cell receptors on their cell surface membranes which bind to complementary antigens.
- The receptors can only recognise antigens which are on the surface of other cells.
20
Q
What are 4 examples in which T cells can recognise antigens (on the surface of other cells)
A
- When the cell is infected with a virus: Antigens from virus are presented on the surface of the infected cell.
- Mutations in normal body cells which can turn into cancer cells: cancer cells produce abnormal proteins which are not usually produced by healthy cells.
- Transplanted cells.
- After phagocytosis.
21
Q
What is the role of T Helper cells
A
- T helper cell with the correct T cell receptor binds to the surface antigen.
- This activates the T helper cell and it undergoes mitosis which produces identical clones.
- Activated T helper cells release chemical signals (cytokine molecules called interleukins): stimulate phagocytes to increase their rate of phagocytosis, stimulate B cells to divide by mitosis and activate cytotoxic T cells.
22
Q
What is the role of Cytotoxic T cells
A
- Identify abnormal or virally infected cells.
- They attach to the cell and release perforin protein which creates holes in the cell surface membrane.
- The cell is now freely permeable to all substances - causes cell to die as water leaves so no metabolic reactions can take place.
23
Q
What is the role of T Memory cells
A
- Formed from the T helper cells which have T cell receptors that are complementary to that specific antigen, so speeds up process of fighting infection.
- They recognise the antigen from last time and can rapidly differentiate into cytotoxic T cells (part of secondary immune response).
- Also quickly stimulate the production of B cells (antibodies produced quicker).
24
Q
What are the 2 main types of B cells
A
Plasma cells and memory cells.
25
What is the role of B plasma cells
They secrete specific antibodies that respond to and are complementary to a specific antigen.
26
Describe the humoral response
- T helper cell binds to APC which activates it.
- Activated T helper cell stimulates specific B cells to divide by mitosis.
- Clones of identical B cells produced (clonal selection).
- Results in Plasma and memory cells.
- Plasma cells produce the specific antibody that is complementary to the antigen (monoclonal antibodies).
27
What is the primary immune response
- Responding to a newly encountered antigen.
- B lymphocytes that have specialised into plasma cells secrete lots of antibodies (specific to antigen).
- These plasma cells are short lived (numbers drop off after several weeks) but the antibodies stay in the blood for a long time.
- Other B cells become memory cells that remain in the body for a long time.
- Relatively slow process.
28
How does the secondary immune response work (memory cells)
- Memory cells circulate in blood/tissue fluid.
- When they encounter the same/complementary antigen again, they divide rapidly by mitosis to produce more memory and plasma cells.
29
Describe the secondary immune response
- Infection of same pathogen.
- Memory cells more likely to bind with the antigens within a shorter duration (detected quicker).
- Activates them and they rapidly divide by mitosis.
- Causes greater concentration of antibodies in the blood (more plasma cells).
- Response is greater and more rapid, immune system destroys pathogen before symptoms arise.
30
What is the lymphatic system
- Lymph fluid, nodes (glands) and vessels.
- Acts as a one way drainage system transporting fluid from body tissues into the blood.
- Contains lymphocytes (WBC).
- Gets rid of waste products produced by cells.
31
Describe the structure of an antibody
- Y shaped molecule with 4 polypeptide chains (2 heavy, 2 light).
- Have a constant region which it uses to bind to phagocytes and a variable region which is specific to each antibody.
- The antigen binding sites (part of variable region) have a specific tertiary structure which is complementary to the antigen it binds to.
32
How do antibodies fight infection
- They bind to the antigen on the surface of the pathogen so it can no longer invade host cells.
- Can also bind to endotoxins (toxins produced by pathogens) and neutralise them.
33
What is agglutination
- Antibodies can bind to multiple antigens at a time and clump them into one big group.
- This group cannot infect cells which makes it easy for phagocytes to engulf multiple pathogens at once.
34
What are monoclonal antibodies and how can they be used.
- Identical antibodies cloned from a specific B/ Plasma cell.
- Can be used in science and medicine as a therapeutic drug or for a medical diagnosis.
35
What is direct monoclonal antibody therapy (e.g. for a cancer cell)
- Specific antigen on cancer cell.
- Specific monoclonal antibodies can be given to a patient with a specific cancer.
- Antigen antibody complexes form.
- Cancer cell can no longer replicate/ grow at an uncontrolled rate.
36
What is indirect monoclonal antibody therapy
- Antibodies can be tagged with a radioactive or cytotoxic drug.
- Antigen antibody complexes formed.
- Once bound, the drug will destroy the cancer cell.
37
What is an ELISA test
- Enzyme linked immunosorbant assay.
- Uses monoclonal antibodies to test for the presence of antigens or antibodies.
- Can be used to rapidly diagnose things like pregnancy, HIV, chlamydia, etc.
38
ELISA test example: describe how HIV could be detected
- Patients with HIV will have antibodies present in their blood (within a few weeks).
- HIV antigen is attached to a plate.
- Sample of patients blood is added which causes antigen-antibody complexes to form (if person has HIV and antibodies are present).
- Plate is washed to remove any unbound antibodies.
- A specific enzyme-labelled antibody is added (secondary antibody) which binds to the primary antibody-antigen complex.
- Colourless substrate is added to the enzyme.
- Enzyme hydrolyses substrate which changes colour, indicating a positive result.
- Can also be other way round (antibody on plate, antigen binding from blood).
39
ELISA test example: describe how pregnancy tests work
- Pregnant women contain high concentrations of hCG hormone in their urine.
- Urine contacts dipstick (testing part).
- Dipstick contains hCG antibodies with a blue latex particle attached.
- hCG binds to antibody (if present).
- Antibodies move up dipstick.
- A row of antibodies immobilised at this point bind to the antigen-antibody complex.
- Blue line in this position = positive result.
- A row of antibodies immobilised at this point bind to antibodies without hCG attached.
- Blue line here only = negative (control line).
40
What is the purpose of control lines on testing kits
Prevents false negatives as it shows the antibodies have moved up the whole strip.
41
Why are monoclonal antibodies considered unethical
- Involve animal testing (mice/rats/rabbits, e.g): They are deliberately infected with an antigen/ pathogen which deliberately causes harm.
- Side effects/ risks: there have been cases where monoclonal antibodies have caused multiple organ failure and death (very occasionally).
42
What does HIV and AIDS stand for
- Human immunodeficiency virus.
- Aquired immunodeficiency syndrome.
43
Describe the structure of the HIV virus and what type of virus is it.
- Retrovirus as it contains RNA.
- has a lipid envelope, attachment proteins, capsid (protein layer), 2 RNA strands and enzymes.
- Has reverse transcriptase enzyme which catalyses the production of DNA from RNA.
44
How is HIV transmitted
- When the bodily fluids of a HIV positive person mix with the bodily fluids of a HIV negative person.
- E.g. sexual intercourse, blood transfusions, intravenous drug users (e.g. heroine), infected mother passes to baby.
45
Describe the life cycle/ how HIV reproduces
- HIV enters bloodstream and circulates.
- HIV proteins binds to CD4/ specific proteins found primarily on T helper cells.
- Capsid fuses with the cell surface membrane of the T helper cells, allowing RNA and enzymes from the HIV virion (singular virus molecule) to enter the T helper cell.
- HIV reverse transcriptase: Virus's RNA => DNA.
- Virus DNA inserted into T helper cell's DNA.
- T helper cell replicates Virus DNA like it would its own (semi-conservative replication).
- Protein synthesis creates new viral components (e.g. enzymes and attachment proteins).
- Virus components assembled into new virus particles.
- New HIV particles leave the cell (budding or lysis) taking some of the cell surface membrane with it to form the lipid envelope.
- Replication of HIV often goes into dormancy and years later it can lead to AIDS.
46
What is AIDS
- When HIV replicates, T cell numbers decline.
- T cells needed for cell mediated immunity.
- The body can no longer respond to infections or cancerous cells.
47
How does AIDS affect the body
- No Tells, so no stimulation of cytotoxic T cells and B cells so no antibodies prooduced.
- Memory cells can become infected and destroyed.
- AIDS sufferers often develop lung, intestine, brain and eye infections.
- HIV doesn't directly cause death, but these secondary infections do.
48
Why are antibiotics inaffective against viruses like HIV
- Antibiotics inhibit enzymes required to form the murein cell walls on bacteria cells.
- This weakens cell walls so they can't withstand osmotic pressure, so water enters via osmosis causing the cell to burst and the bacterium dies.
- Doesn't work on viruses as they don't have cell walls.
49
What is the difference between B plasma cells and B memory cells
- B plasma cells: short-lived, secrete specific monoclonal antibodies, involved in primary and secondary immune response.
- B memory cells: longer lived, don't secrete antibodies and involved only in secondary immune response.
50
How does antigen variability occur
- Mutations in DNA/RNA cause antigens produced on the pathogens surface to constantly change (changes in amino acid sequence could cause different tertiary structure).
- If it changes enough, a new strain has developed.
- This causes the primary immune response to begin as receptors on memory cells are no longer complementary.
51
What is passive immunity
When we did not encounter the antigen, but get ready made antibodies for it (e.g. passed down from mother through placenta or breast milk, anti-venom for snake bites).
52
What are advantages and disadvantages of passive immunity
- A: Immediate protection (don't have to spend time making antibodies).
- D: No memory cells, so no long-lasting immunity.
53
What is active immunity
Produced by stimulating the production of antibodies by the individuals own immune system (have encountered a version of the antigen).
54
What is natural active immunity
Become infected, body produces its own antibodies.
55
What is artificial active immunity
- Vaccination/ immunisation.
- An immune response is created but no symptoms occur.
56
What are advantages and disadvantages of artificial immunity
- A: Long lasting immunity.
- D: Takes time to develop immunity.
57
How do vaccinations work
- Antigen binds to surface receptors on specific T cell.
- T cell stimulates/ activates a specific B cell (that secretes the correct antibodies).
- B cell divides by mitosis to produce plasma and memory cells.
- B plasma cells secrete the specific antibody.
- (Some) B cells become memory cells.
- Memory cells produce larger amounts of plasma cells/ antibodies faster when the antigen is encountered again.
58
What is herd immunity
A large proportion of the population are vaccinated to prevent the spread of a pathogen.
59
Why is herd immunity useful
Some people cannot be vaccinated (e.g. babies, very young children, those who are ill or have compromised immune systems).
60
What are ethical issues of vaccines
- Involve the use of animals.
- Side effects (though rare) can cause long term harm.
- Expensive to conduct research into creating vaccines.
- Question of who should be tested on and how trials should be carried out.
- Herd immunity makes them the most successful, but question of whether or not they should be compulsory.
