2C - Cells And The Immune System Flashcards
1
Q
What are antigens?
A
Proteins on the surface of cells that can generate an immune response when detected by the body.
2
Q
What can antigens allow the body to recognise?
A
- Pathogens
- Abnormal body cells
- Toxins
- Cells from other individuals of the same species
3
Q
What are pathogens?
A
Organisms that cause disease.
4
Q
What is the difference between T-cells and T-lymphocytes?
A
Nothing, they are the same thing (a type of white blood cell).
5
Q
Are specific lymphocytes produced in response to an infection?
A
- No, they all already exist.
- There are many different types -> Only a few will match the pathogen’s antigens.
- The ones that match are stimulated to divide -> Clonal selection.
6
Q
What are the types of defence mechanism against infection?
A
- Non-specific -> Physical barrier + Phagocytosis
* Specific -> Cell-mediated response + Humoral response
7
Q
What is the difference between the non-specific and specific immune response?
A
- Non-specific -> Immediate and the same for all pathogens
* Specific -> Slower and specific to each pathogen
8
Q
What are the different types of white blood cell?
A
- Phagocytes
* Lymphocytes -> T-cell + B-cell
9
Q
What are phagocytes?
A
A type of white blood cell that ingest and destroy pathogens (phagocytosis).
10
Q
What are lymphocytes?
A
White blood cells involved in the specific immune response.
11
Q
What is phagocytosis?
A
The process by which phagocytes engulf and digest pathogens.
12
Q
Describe the process of phagocytosis.
A
1) Phagocyte is attracted to the pathogen by its chemical products + moves along the concentration gradient towards it.
2) Phagocyte attaches onto the pathogen’s antigens.
3) Cytoplasm moves around the pathogen + forms a phagosome.
4) Lysosomes in the phagocyte migrate towards the phagosome and release lysozymes into it.
5) Lysosomes hydrolyse the pathogen + the products are absorbed by the phagocyte.
6) Phagocyte displays antigens on the cell surface to activate other cells.
13
Q
What is a phagosome?
A
The “bubble” that is formed around the pathogen when a phagosome engulfs it.
14
Q
What are lysosomes and lysozymes?
A
- Lysosomes -> Sacs that contain lysozymes.
* Lysozymes -> Enzymes that break down (hydrolyse) forgein material.
15
Q
Compare how quickly non-specific and specific immune response happens.
A
Non-specific is faster, but specific provides long-term immunity.
16
Q
What is another name for B lymphocytes?
A
B cells
17
Q
What is another name for T lymphocytes?
A
T cells
18
Q
Are phagocytes and lymphocytes part of the specific or non-specific immune response?
A
- Phagocytes -> Non-specific
* Lymphocytes -> Specific
19
Q
Where are lymphocytes produced?
A
By stem cells in the bone marrow.
20
Q
What is the cellular immune response?
A
The T-cells and other immune system cells that they interact with -> e.g. Phagocytes
21
Q
What is the humoral immune response?
A
B-cells, clonal selection and the production of monoclonal antibodies.
22
Q
What type of cells is the cellular immune response associated with?
A
T-cells
23
Q
What type of cells is the humoral immune response associated with?
A
B-cells
24
Q
What are the two parts of immune response?
A
- Cellular
* Humoral
25
What is another name for cellular response?
Cell-mediated response
26
How can T-cells distinguish harmful cells and pathogens from normal body cells?
* Phagocytes that have engulfed and hydrolysed a pathogen present some of a pathogen’s antigens on their own membrane
* Body cells invaded by a virus present some of the viral antigens on their membrane
* Transplanted cells from the same species have different antigens on their membrane
* Cancer cells present antigens on their membrane
27
What do T-cells do in the immune response?
• Receptor proteins on the helper T-cell surface bind to complementary antigens presented by phagocyte
• This activates the helper T-cell to divide by mitosis.
• Cloned cells:
1) Become memory T-cells -> Allow rapid response in the future
2) Stimulate phagocytosis
3) Stimulate B cells to divide and secrete antibodies
4) Activate cytotoxic T cells
28
Which T-cells are first to respond in the immune response?
Helper T-cells
29
Are all helper T-cells the same?
* No, each type has different receptors that respond to a different antigen.
* Only the ones that bind to the antigen presented by the phagocytes divide by mitosis.
30
What do cytotoxic T-cells do?
* Produce a protein called perforin
| * Perforin makes holes in the cell-surface membrane
31
What protein do cytotoxic T-cells make?
Perforin
32
Describe the entire cellular immune response.
PHAGOCYTES:
• Phagocytes engulf and digest pathogens by phagocytosis
• Present antigens on their surface
HELPER T-CELLS:
• Receptor proteins on surface bind to complementary antigens presented by phagocyte
• This activates the helper T-cell to divide by mitosis.
• Cloned cells:
1) Become memory T-cells -> Allow rapid response in the future
2) Stimulate phagocytosis
3) Stimulate B cells to divide and secrete antibodies
4) Activate cytotoxic T cells
CYTOTOXIC T-CELLS:
• Produce perforin
• Perforin produces holes in cell membranes
33
Name the types of cell involved in the cellular immune response.
• Phagocyte
• Helper T-cell
• Cytotoxic T-cell
(• Memory T-cell)
34
Are are B-cells the same?
* No, each type has different antibodies on its surface.
* Only the ones that produce (and have on their surface) the antibody that is complementary to the pathogen’s antigens will be activated by helper T-cells to divide.
35
What do B-cells do in the cellular immune response?
• Antigens on the pathogen bind to complementary antibodies that cover the B-cell
• Antigens are engulfed by the B-cell by endocytosis + presented on the cell surface
• Helper T-cells bind to the antigen on the cell-surface and activate the B-cell
• B-cell divides by mitosis to form plasma cells or memory cells (clonal selection)
PLASMA CELLS (Primary response):
• All produce the antibody that is specific to the foreign antigen
• Antibodies
MEMORY CELLS (Secondary response):
• Allow a faster immune response in case of second infection
• Do not produce antibodies but rapidly divide to give plasma and memory cells if encounter the antigen
36
What is clonal selection?
*Check with teacher*
The process by which a B-cell with the specific antibody for a particular antigen is stimulated to divide and the body can produce antibodies for that antigen rapidly.
37
Name the types of cells involved in the humoral immune response.
• B-cell (+ plasma cell)
| • Memory B-cell
38
What are plasma cells?
* Cloned versions of a B-cell, produced when a specific B-cell is stimulated to divide.
* Produce monoclonal antibodies that are specific to an antigen.
* Have a short lifespan.
39
What is the difference between memory T-cell and memory B-cells?
*Ask teacher*
40
What are memory B-cells?
* Cloned versions of a specific B-cell
* Allow a quick response in case of second infection -> Do not produce antibodies but rapidly divide to give plasma and memory cells if encounter the antigen
* Have a long lifespan.
41
Describe the entire humoral immune response.
B-CELLS:
• Antigens on the pathogen bind to complementary antibodies that cover the B-cell
• Antigens are engulfed by the B-cell by endocytosis + presented on the cell surface
• Helper T-cells bind to the antigen on the cell-surface and activate the B-cell
• B-cell divides by mitosis to form plasma cells or memory cells (clonal selection)
PLASMA CELLS (Primary response):
• All produce the antibody that is specific to the foreign antigen
• Antibodies
MEMORY CELLS (Secondary response):
• Allow a faster immune response in case of second infection
• Do not produce antibodies but rapidly divide to give plasma and memory cells if encounter the antigen
42
Describe the entire immune response.
PHAGOCYTES:
• Phagocytes engulf and digest pathogens by phagocytosis
• Present antigens on their surface
HELPER T-CELLS:
• Receptor proteins on surface bind to complementary antigens presented by phagocyte
• This activates the helper T-cell to divide by mitosis.
• Cloned cells:
1) Become memory T-cells -> Allow rapid response in the future
2) Stimulate phagocytosis
3) Stimulate B cells to divide and secrete antibodies
4) Activate cytotoxic T cells
CYTOTOXIC T-CELLS:
• Produce perforin
• Perforin produces holes in cell membranes
B-CELLS:
• Antigens on the pathogen bind to complementary antibodies that cover the B-cell
• Antigens are engulfed by the B-cell by endocytosis + presented on the cell surface
• Helper T-cells bind to the antigen on the cell-surface and activate the B-cell
• B-cell divides by mitosis to form plasma cells or memory cells (clonal selection)
PLASMA CELLS (Primary response):
• All produce the antibody that is specific to the foreign antigen
• Antibodies
MEMORY CELLS (Secondary response):
• Allow a faster immune response in case of second infection
• Do not produce antibodies but rapidly divide to give plasma and memory cells if encounter the antigen
43
Remember to practice drawing out a flowchart for the entire immune response.
Textbook pgs 104-110 + Revision guide pg 44
44
What are antibodies?
* Proteins with specific binding sites produced by B-cells.
| * Bind to antigens to produce antigen-antibody complexes.
45
What type of molecule are antibodies?
Proteins
46
What happens when an antibody binds to antigen?
* Antigen-antibody complex forms
| * If an antibody binds to two antigens, they clump together -> Agglutination
47
Describe the structure of an antibody.
* 2 long inner HEAVY chains
* 2 shorter outer LIGHT chains
* Variable regions at the top of each chain -> Binding site between the tops of a light and heavy chain
48
What joins the two heavy chains in an antibody?
Disulfide bridge
49
What causes the two heavy chains in an antibody to bend?
Hinge protein
50
Where are the constant and variable regions in an antibody?
* Constant -> Bottom parts of each chain
| * Variable -> Top parts of each chain
51
How many binding sites are on an antibody?
| Are they the same?
* 2
| * Yes
52
In an antibody, are the light or heavy chains longer?
Heavy
53
Where are the binding sites on an antibody?
At the variable regions at the top of each pair of chains.
54
What are the 4 chains in an antibody?
Polypeptide chains
55
What determines the specificity of an antibody?
The tertiary structure of the variable region of the polypeptide chains.
56
Is the constant region the same in each antibody?
Yes
57
Remember to practise labelling an antibody.
Pg 44 of revision guide.
58
Do antibodies destroy antigens?
No, they prepare the antigen for destruction.
59
How do antibodies help in the immune response?
1) Bind to two pathogens at once -> Agglutination -> Allows phagocytes to phagocytose many pathogens at once
2) Serve as markers that stimulate phagocytes to engulf the cells they are attached to
60
What are monoclonal antibodies?
Antibodies produced from a single group of genetically identical B-cells.
61
What is the primary immune response?
* The immune response when an antigen enters the body for the first time.
* Involves the production of antibodies and memory cells.
* It is slow.
62
What is the secondary immune response?
* The immune response that occurs when an antigen enters the body for the second time.
* Involves memory B-cells dividing into plasma cells and memory T-cells dividing into the correct type of T-cells.
* It is fast.
63
Explain the difference in speed of the primary and secondary response.
* Primary -> Slow -> Aren’t many B-cells that can make the antibody needed.
* Secondary -> Fast -> Memory B-cells and memory T-cells are ready to divide and fight the disease -> Antibodies produced faster.
64
Will there be symptoms during the primary and secondary immune response?
* Primary -> Yes
| * Secondary -> Probably not
65
How do memory B-cells and memory T-cells work when activated?
* Memory B-cells -> Divide into plasma cells and memory B-cells -> Plasma cells produce the right type of antibody
* Memory T-cells -> Divide into the correct type of T-cells to kill the cell carrying the antigen
66
What causes the secondary immune response to be different from the primary?
* The primary immune response involves producing memory T-cells and memory B-cells.
* These allow for a faster secondary immune response.
67
What is immunity?
A system’s ability to quickly respond to a specific infection before it can cause harm.
68
Describe the graph for “concentration of the right antibody in the blood” (y) against time (x) for the primary and secondary response.
Primary response:
• Slower response after exposure -> Peak rises after more days + slow rise
• Lower peak height
• Doesn’t necessarily fall back to near 0 antibody concentration
Secondary response:
• Quicker response after exposure -> Peak rises after fewer days + more sharply
• Higher peak height
69
Remember to revise antibody graphs for primary and secondary immune response.
See diagram pg 45 of revision guide.
70
What is vaccination?
The introduction of a specific disease antigen into the body in order to stimulate an immune response against a particular disease.
71
How does a vaccine work?
* Antigens (or dead pathogens) for a particular disease are injected into a human
* This prompts the primary immune response.
* Memory cells are produced.
* These allow a faster response next time an infection occurs -> Antibodies produced quicker.
72
What is herd immunity?
When a large percentage of the population is vaccinated, the rest of the population is also less likely to catch the disease since there are fewer people to catch it from.
73
What are the two ways a vaccine can be done?
* Orally
| * Injection
74
What is the disadvantage of taking a vaccine orally?
It may be broken down by enzymes in the gut or the molecules of the vaccine may be too large to be absorbed into the blood.
75
Why are booster vaccinations given?
To boost the levels of memory cells.
76
How may the antigens in a vaccine be made harmless?
* Free antigens
* Dead pathogen
* Weakened pathogen
77
What is antigenic variation and what is the effect of this?
* When a pathogen mutates frequently, so that the antigens on its surface change.
* If you are infected for a second time, your memory cells from the first infection will not recognise the different antigens -> Primary response happens again.
78
How does antigenic variation affect the use of vaccines?
* It makes developing vaccines for certain diseases difficult.
* Sometimes a new vaccine may be required each year.
79
Give 2 examples of pathogens that show antigenic variation.
* HIV
| * Influenza
80
What is the term for different strains of a disease that emerge each year as a result of antigenic variation?
Immunologically distinct strains
81
Describe how and why a vaccine for influenza is produced.
* The influenza virus shows antigenic variation and mutates to form new strains each year.
* The antigens on the surface of each strain are different.
* So memory cells produced by vaccination with one strain will not recognise other strains.
* Each year there are many strains of influenza circulating, so a new vaccine has to be made and chosen each year.
* Governments and health authorities implement a programme of vaccination.
82
Explain why certain pathogens change their surface antigens frequently.
* The pathogen may mutate.
* Different genes cause different antigens to be present on he cell surface.
This is known as antigenic variation.
83
What factors determine how successful a vaccination programme is?
* Economically viable to immunise most of population
* Few side-effects
* Means of producing, storing and transporting the vaccine
* Means of administering vaccine
* Ability to vaccinate majority of population -> Herd immunity
84
Why may a vaccine not eliminate a disease?
* Vaccine fails to induce immunity in certain individuals
* Individuals may develop disease immediately after vaccination (before immunity levels are high enough to prevent it)
* Antigenic variation
* Too many varieties of a particular pathogen (e.g. over 100 varieties of common cold)
* Certain pathogens “hide” from the body’s immune system (e.g. by hiding in cells)
* Individuals may object to vaccine for religious, ethical or medical reasons
85
What are the two types of immunity?
* Active
| * Passive
86
What is active immunity?
The type of immunity you get when your immune system makes its own antibodies after being stimulated by an antigen.
87
What is passive immunity?
* The type of immunity you get from being given antibodies made by a different organism.
* Your body doesn’t produce any antibodies of its own.
88
What are the two types of natural immunity?
* Natural
| * Artificial
89
What are the two types of passive immunity?
* Natural
| * Artificial
90
What is the difference between natural and artificial active immunity?
* Natural -> When you become immune after catching a disease.
* Artificial -> When you become immune after a vaccination.
91
What is the difference between natural and artificial active immunity?
* Natural -> When a baby becomes immune due to the antibodies it receives from its mother, through placenta and in breast milk.
* Artificial -> When you become immune after being objected with antibodies from someone else.
92
What type of immunity is it when you catch a disease and then become immune to it?
Natural active immunity
93
What type of immunity is it when you’re given a vaccination?
Artificial active immunity
94
What type of immunity is it when a baby becomes immune due to antibodies it receives from its mother?
Natural passive immunity
95
What type of immunity is it when anti-venom is given to someone who has suffered a snake bite?
Artificial passive immunity
96
What are the differences between active and passive immunity?
* Active requires exposure to antigen, while passive doesn’t
* Active takes time to develop, while passive is immediate
* Active produces memory cells, while passive doesn’t
* Active offers long-term protection, while passive doesn’t
97
Compare how immediate active and passive immunity are.
* Active -> Takes time to develop
| * Passive -> Immediate
98
Compare whether memory cells are produced in active and passive immunity.
* Active -> Memory cells produced
| * Passive -> No memory cells produced
99
Is active immunity long-term? Why?
* Long-term
| * Because memory cells are produced, which allow antibodies to be quickly produced in the event of an infection
100
Is passive immunity long-term? Why?
* Short-term
| * Antibodies given are broken down + No memory cells produced
101
Remember to revise the different types of immunity.
Pg 47 of revision guide.
102
Why are antibodies very specific?
They have a unique tertiary structure that only one antigen will bind to.
103
Can you make monoclonal antibodies for anything?
Yes
104
Why are monoclonal antibodies useful?
They will bind to only one type of antigen, so a specific type of cell can be targeted.
105
Give some ways in which monoclonal antibodies can be used.
* Targeting specific cell types -> e.g. cancer treatment
* Pregnancy testing
* Medical diagnosis -> e.g. ELISA
106
Describe how monoclonal antibodies can be used to target cancer cells.
1) Cancer cells have antigens called tumour markers that are not found on normal body cells.
2) Monoclonal antibodies that bind to these tumour markers can be made.
3) Anti-cancer drugs are attached to these antibodies.
4) The antibodies bind to and accumulate near cancer cells, allowing the drug to work there.
107
What are specific antigens on cancer cells called?
Tumour markers
108
Why do monoclonal antibody anti-cancer drugs have lower side effects that other drugs?
The antibodies mean that the drugs accumulate near the target cells.
109
Remember to revise how monoclonal antibodies can be used to target cancer cells.
Pg 48 of revision guide.
110
Describe how monoclonal antibodies are used in pregnancy tests.
1) hCG is a hormone found only in the urine of pregnant women.
2) The application area of a pregnancy test contains antibodies for hCG with a blue coloured bead attached.
3) When urine is applied, any hCG will bind to the antibody, forming an antigen-antibody complex.
4) Urine moves up the stick to the test strip, carrying any beads with it.
5) The strip contains antibodies to the hCG that are immobilised.
6) If hCG is present, the immobilised antibody binds to hCG, which also has the blue beads attached to it.
7) This turns the test strip blue.
8) If no hCG is present, the beads pass straight through the test strip without binding, so there is no colour.
111
What hormone are pregnancy tests based on?
hCG
112
What is hCG?
* Human chorionic gonadotropin.
| * A hormone found in the urine of pregnant women.
113
Remember to practice drawing out how a pregnancy test works.
Pg 48 of revision guide.
114
What does ELISA stand for?
Enzyme-linked immunosorbent assay
115
What is ELISA?
A test used to see if a patient has any antibodies to a certain antigen, or any antigen to a certain antibody.
116
What can ELISA be used to test for practically?
* Pathogenic infections
* Allergies
* Anything you can make an antibody for
117
How does ELISA give a positive result?
There is a colour change as a result of the enzyme on the final antibody reacting with a substrate.
118
Does ELISA allow you to work out the quantity of the antigen or antibody being tested for?
* Sometimes
| * The intensity of the colour indicates the quantity.
119
What are the different types of ELISA?
* Direct
| * Indirect
120
Describe indirect ELISA when testing for a specific antigen.
1) Attach monoclonal antibodies complementary to the antigen you are testing for to the base.
2) Add test sample containing antigen.
3) Wash.
4) Add monoclonal antibodies complementary to antigen.
5) Wash.
6) Add antibodies complementary to previous antibodies, with enzymes attached to them.
7) Wash.
8) Substrate added -> Changes colour if enzyme is present -> Positive result.
121
Compare direct and indirect ELISA.
* Direct ELISA -> Uses a single antibody complementary to the antigen being tested for.
* Indirect ELISA -> Uses two different antibodies in a sort of chain.
(See revision guide pg 49 or exercise book)
122
Describe the difference between how ELISA can be used to test for an antigen or antibody.
Testing for an antigen:
• Antibodies attached to base
Testing for an antibody:
• Antigens attached to base
123
How can you tell if a given example of ELISA is direct or indirect?
* If there are two antibodies added above the antigen -> Indirect
* If there is one antibody added above the antigen -> Direct
124
Why must the system in ELISA be washed several times?
* To remove any unbound antibodies from the dish
| * e.g. Unbound secondary antibodies (with the enzyme attached) could give a false positive if not washed out
125
Remember to practise drawing out the difference between direct and indirect ELISA.
Exercise book + pg 49 of revision guide
126
What disease can ELISA be used to detect?
HIV
127
What type of ELISA is used to detect HIV in a sample?
Indirect ELISA
128
When ELISA is used to detect HIV, does it directly test for HIV viruses?
No, it tests for the presence of HIV antibodies that an infected patient would possess.
129
Describe the ELISA test used to test for HIV in a patient.
Indirect ELISA is used:
1) HIV antigen is bound to the bottom of a well in a well plate
2) A sample of the patient’s blood is added to the well.
3) If there are HIV-specific antibodies present, then these will bind to the antigens on the bottom.
4) The well is washed out to remove any unbound antibodies.
5) A secondary antibody that has a specific enzyme attached to it is added -> Can bind to the HIV-specific antibody (primary antibody)
6) The well is washed out to remove any unbound secondary antibody -> All washed out if there’s no primary antibody.
7) A solution is added. It contains a substrate that reacts with the enzyme to give a colour change.
8) If the solution changes colour, it indicates the presence of HIV-specific antibodies in their blood, which shows they’re infected with HIV.
130
Remember to practise drawing out the ELISA process to detect HIV in a patient.
Pg 49 of revision guide
131
When a study presents evidence for a new theory, what is it important to do?
* Scientists come up with more evidence to validate the theory.
* They may repeat the study or conduct other studies.
132
Describe how the MMR vaccine was evaluated by studies.
* In 1998, a study was published that concluded that there may be a link between the MMR vaccine and autism. It was based on 12 children with autism.
* The small sample size increased the likelihood of this being down to chance + there may have been bias as one the scientists was trying to gain evidence for a lawsuit against the vaccine manufacturer. Other studies also found no link.
* In 2005, a Japanese study was published based on 30,000 children. This showed no link between the MMR vaccine and autism.
133
When given data about a vaccine’s effects, what might you be asked to do?
* Describe the data
* Draw conclusions
* Evaluate the methodology
134
Looking at the MMR vaccine graph on pg 50, describe the data.
* Overall the number of children diagnosed with autism per year increased.
* However, this increase continued after the MMR vaccine was stopped.
* There were fluctuations in number over time.
135
Looking at the MMR vaccine graph on pg 50, draw conclusions.
There is no link between the MMR vaccine and autism.
136
Looking at the MMR vaccine graph on page 50, evaluate the methodology.
The sample size was very large (30,000), so it is unlikely that the results were down to chance.
137
Describe what Herceptin is and how it works.
* About 20% of women with breast cancer have tumours that produce more than the usual amount of a receptor called HER2.
* Herceptin is a drug that contains monoclonal antibodies that bind to the HER2 receptor on a tumour cell and prevent cell growth and division.
138
Describe how Herceptin was evaluated by studies.
* In 2005, a study tested Herceptin in women who had already undergone chemotherapy for HER2-type cancer.
* 1694 women took the drug for a year after chemo.
* 1694 women were observed for the same time (control group).
* The results showed that almost twice as many women in the control group developed breast cancer again or died compared to the Herceptin group.
139
Looking at the Herceptin graph on pg 50, describe the data.
Almost twice as many women in the control group developed breast cancer again or ideas compared to the group taking Herceptin.
140
Looking at the Herceptin graph on pg 50, draw conclusions.
A one-year treatment with Herceptin, after chemotherapy, increases the disease-free survival rate for women with HER2-type breast cancer.
141
What are some ethical issues of vaccines?
* Vaccines are tested on animals before humans + animal substances may be used in vaccines
* Testing on humans can be dangerous and risky
* People who refuse the vaccine are protected by herd immunity -> People might think this is unfair
* If there was an epidemic, it would be a difficult decision to choose who would be the first to receive it.
142
Give an example of how testing vaccines on humans can be risky.
A volunteer receiving a new HIV vaccine might have unprotected sex because they think that they’re fully protected and the vaccine may not work.
143
What are some ethical issues of monoclonal antibody therapy?
• Animals are used to produce the cells from which the monoclonal antibodies are produced -> Some people think this is wrong
144
Remember to practise interpreting vaccine and antibody data.
Pg 50 of revision guide.
145
What does HIV stand for?
Human immunodeficiency virus
146
What is HIV?
* Virus that affects the immune system
| * Leads to AIDS (acquired immune deficiency syndrome)
147
What does AIDS stand for?
Acquired immune deficiency syndrome
148
What is AIDS?
* Condition where the immune system deteriorates and eventually fails
* Makes the person more vulnerable to other infections, like pneumonia.
149
What cells does HIV infect?
Helper T-cells
150
What role do helper T-cells play in a HIV infection?
They are the host cells.
151
How does HIV cause problems?
* Infects helper T-cells
* These usually activate phagocytes, cytotoxic T-cells and B-cells, but now cannot do this.
* Without enough T-cells, immune system can’t mount an effective response to infections, because other immune systems cells don’t behave how they should.
152
When does HIV lead to AIDS?
When the helper T-cell number in the body drops below a critical level.
153
Describe the structure of HIV.
* Core in middle containing genetic material (RNA) and some proteins, including reverse transcriptase
* Outer coating around core called a capsid
* Extra outer layer called envelope -> Made from stolen membrane of past host cell
* Attachment proteins sticking out
154
Name the main parts of a HIV virus.
* Genetic material
* Reverse transcriptase
* Capsid
* Envelope
* Attachment protein
155
What is the genetic material in HIV?
RNA
156
What important enzyme is found in the core of HIV?
Reverse transcriptase -> Needed for virus replication
157
What is the capsid in HIV?
An outer coating of protein around the core.
158
What is the envelope in HIV and what is it made of?
* An extra outer layer, outside the capsid
| * Made of the cell membrane of the previous host cell
159
What are the attachment proteins used for in HIV?
Attaching to the host helper T-cell.
160
Are the attachment proteins on HIV the same?
Yes, they are copies of one attachment protein.
161
Remember to practise labelling the structure of HIV.
Pg 52 of revision guide.
162
Where do viruses reproduce?
Inside host cells.
163
Does HIV replicate on its own?
No, it uses the mechanism of the host cell.
164
Describe how HIV replicates.
1) Attachment protein attaches to receptor molecule on cell membrane of host helper T-cell.
2) Capsid is released into cell, where it uncoats and released the genetic material (RNA) into the cytoplasm.
3) Reverse transcriptase is used to make a complementary strand of DNA from the viral RNA template.
4) From this, double-stranded DNA is made and inserted into the human DNA.
5) Host cell enzymes used to make viral proteins from the viral DNA found within the human DNA.
6) Viral proteins assembled into news viruses, which bud from the cell and infect other cells.
165
Remember to practise drawing out the HIV replication process.
See diagram pg 52 of revision guide.
166
Describe the different stages of a HIV infection.
* After initial injection -> HIV replicates rapidly and infected person may experience severe flu-like symptoms
* After this -> Latency period -> No symptoms
167
What is the latency period?
The period after the initial infection with HIV, where the person does not experience any symptoms.
168
When is a person classed as having AIDS?
• When symptoms of their failing immune system start to appear
OR
• Helper T-cell count drops below a certain level
169
What is the typical time between a HIV infection and the development of AIDS?
About 10 years
170
Does AIDS kill you directly?
No, it makes you more susceptible to other diseases that can kill you.
171
What are the initial symptoms of AIDS?
Minor infections of mucous membranes and recurring respiratory infections.
172
Give an example of initial symptoms of AIDS.
Minor infections of:
• Inside of the nose
• Ears
• Genitals
173
Give an example of mid-stage AIDS symptoms.
* Chronic diarrhoea
* Severe bacterial infections
* Tuberculosis
174
Give an example of late stage AIDS symptoms.
* Toxoplasmosis of the brain (parasite infection)
| * Candidiasis of the respiratory system (fungal infection)
175
Describe how the symptoms of AIDS develop in each stage.
* Initial symptoms -> Minor infections of mucous membranes and recurring respiratory infections
* Mid-stage -> More serious infections, such as chronic diarrhoea, severe bacterial infections and TB
* Late stage -> Range of serious infections, including toxoplasmosis of the brain and candidiasis of the respiratory system
176
What factors affect the progression of HIV to AIDS and survival time with AIDS?
* Existing infections
* The strain of HIV
* Age
* Access to healthcare
177
Do antibiotics kill bacteria and viruses?
* Bacteria -> Yes
| * Viruses -> No
178
How do antibiotics kill bacteria?
* Target the bacterial enzymes and ribosomes
| * This interferes with their metabolic reactions.
179
Do antibiotics damage human cells and why?
* Antibiotics are designed to target the bacterial enzymes and ribosomes
* Bacterial enzymes and ribosomes are different to human ones
* So antibiotics don’t damage human cells
180
Why don’t antibiotics work against viruses?
* Antibiotics target enzymes and ribosomes
* Viruses don’t have their own enzymes and ribosomes (they use those in their host cell’s)
* So antibiotics can’t inhibit them since they can’t inhibit human processes
181
Instead of antibiotics, what is used to combat viruses?
Antiviral drugs
182
How do antiviral drugs work?
* Target virus-specific enzymes.
| * e.g. Reverse transcriptase, which is needed for HIV replication
183
Do antiviral drugs affect humans? Why?
No, because they target virus-specific enzymes, so they don’t affect the host cell.
184
What type of drug is used to treat HIV?
* Reverse-transcriptase inhibitors
| * These stop HIV replication by inhibiting reverse transcriptase, without affecting the host cell.
185
What are reverse-transcriptase inhibitors used for?
Stopping HIV replication by inhibiting reverse transcriptase.
186
Is there a cure or vaccine for HIV?
No, but there are antiviral drugs to slow its progression.
187
What is the best way to control HIV?
Reducing its spread by unprotected sex, etc.
188
How can HIV spread?
* Unprotected sex
* Infected bodily fluids
* From HIV-positive mother to fetus
189
Are all babies from a HIV-positive mother also HIV-positive?
No, and taking antiviral drugs during pregnancy can decide the chance of the baby being HIV-positive.
190
Is HIV testing before 18 months accurate?
No, because a baby from a HIV-positive mother may have some HIV antibodies in their blood, regardless of whether they’re infected.
