Give one get one…

In pairs name as many diseases as you can, one at a time. First person
to umm, ahh or pause loses!!
 Synoptic:
• Have you been taught anything that relates to immunology so far on
your biology course?
WBC’s engulf
bacteria by
phagocytosis
Antibodies are Lysosomes fuse with the
globular Glycoproteins & vacuole and release
proteins glycolipids act in digestive enzymes to
cell – cell destroy the bacterium
recognition
Stomach acid
helps to kill
many
microorganisms All viruses cause
Goblet cells in the trachea
harm, only some
produce mucus to trap
bacteria do
microorganisms. Cilia waft
to remove this mucus.
Immunology

Lesson objectives
• Define immunology key terms
• Understand and explain that the body is a host to many organisms
• Describe characteristics of a few key diseases – cholera, tuberculosis,
smallpox, influenza & malaria
An organism that causes damage to it’s host
Pathogen
A disease that may be passed or transmitted
from one individual to another
Infectious
A person who shows no symptoms when
infected by a disease organism but can pass the
disease on to another individual
Carrier
Where a pathogen is normally found; this may
be in humans or another animal and may be a
source of infection
Disease reservoir
A disease which is always present at low levels in an area.
Endemic
Where there is a significant increase in the usual number
of cases of a disease, often associated with a rapid
disease spread.
Epidemic
An epidemic occurring worldwide, or over a very wide
area, crossing international boundaries and usually
affecting a large number of people.
Pandemic
Uses non-pathogenic forms, products or antigens of
micro-organisms to stimulate an immune response which
confers protection against subsequent infection.
Vaccine
Substances produced by microorganisms which affect the
growth of other microorganisms.
Antibiotics

Where a microorganism, which should be affected by an

antibiotic, is no longer susceptible to it.
Antibiotic resistance
A living organism which transfers a disease from one
individual to another.
Vector
A chemical produced by a microorganism which causes
damage to its host.
Toxin
Organisms with the same or very similar antigens on the surface. Such types are
sub-groups or strains of a microbial species which may be used to treat
infections. They are usually identified by using antibodies from serum.
Antigenic types

A molecule that causes the immune system to produce antibodies against it.
These may be individual molecules or those on the surface of cells.
Antigen
The key organs of the immune system include:
1.Bone marrow: where all blood cells are initially formed including the white blood cells, i.e.
the leucocytes, of which there are two categories: granulocytes and agranulocytes
2.Thymus gland: where special leucocytes called T lymphocytes mature

Synoptic: Briefly describe the difference between granulocytes and agranulocytes:

• Granulocytes have a lobed nucleus and granular cytoplasm containing
lysosomes. They engulf pathogens (by phagocytosis).
• Agranulocytes do not have granules (clear cytoplasm) and have a spherical
nucleus. They tend to secrete antibodies.
Disease: The body as a host
Even though we have approximately 1013 cells in our bodies, we have many
more of other organisms living in or on the body. They include microbes such
as fungi, protoctista and bacterial species. Many of these organisms cause
disease, such as by secreting toxins. Many organisms though contribute to our
health and we are said to have a mutualistic relationship.

Escherichia coli in the large intestine synthesises vitamin K where it is

absorbed by the body (needed for correct blood clotting and carriage of
Ca2+ to help build strong bones). How might bacteria benefit from
humans?
• Gain products of digestion that the host couldn’t digest/absorb e.g.
cellulose
• Protection
• Optimum temperature and pH
HW Research TASK
• You are to produce an informative and eye-catching disease fact file for one of
the below diseases:
• Cholera
• Tuberculosis
• Influenza
• Malaria
Success Criteria
You must provide information on:
1. The organism that causes the
disease
2. The mode of transmission
3. Symptoms
4. Treatment if infected
5. Prevention methods
Let’s see how informative your fact file is!
• Swap your fact file with someone else in the room (choose someone
who chose a different disease to you if possible).
• You are to mark your peers fact file using the template provided.
Fact File Feedback
• Is information provided on the organism that causes
disease?

• Are symptoms of the disease described?

• Are treatment methods described?

• Do you understand how this disease is transmitted?

• Are prevention methods described?

• Does the fact file look eye-catching?

Comment on overall strengths:

What could they do to improve?

Important diseases
You need to know about some important diseases:

Cholera Tuberculosis
Smallpox

Influenza Malaria
TASK:
• Use the fact files around the room to learn lots of exciting science
about the 5 key diseases on your specification!
• Make notes on page 4/5 of your booklet.
Cholera https://youtu.be/8-sqticNg5o

Name of pathogen
Vibrio cholerae
Type of pathogen
Gram negative bacterium
Site of infection and symptoms
Toxins affect the human gut lining causing a watery diarrhoea, severe
dehydration and frequently death.
Source and mode of transmission
Humans act as reservoirs or carriers and contaminate water supplies in
which the organism is transmitted, although it only multiplies in the human host.
Prevention and control
Treatment of water, good hygiene and provision of
clean drinking water.

Vaccine may provide temporary protection.

Treatment
Antibiotic treatment is possible but rehydration is the main part of treatment.
Tuberculosis https://www.cdc.gov/tb/topic/basics/default.htm

Name of pathogen
Mycobacterium tuberculosis
Type of pathogen
Bacterium
Site of infection and symptoms
Most commonly affects lung & neck lymph nodes.
Symptoms include coughing, chest pain & coughing up blood.
Source and mode of transmission
It can be spread rapidly in overcrowded conditions and is transmitted in airborne
droplets through coughing and sneezing of infected individuals in close proximity.
Prevention and control
BCG vaccination programme for children.

Treatment
A long course of antibiotics.
Small Pox
Name of pathogen
Virola major
Type of pathogen
Virus
Site of infection and symptoms
Small blood vessels of the skin, mouth & throat causing a rash &
blisters. 30 to 60% fatality rate.
Source and mode of transmission
Airborne droplets of infected individuals in close proximity.
 https://youtu.be/E_PKQ_M7AtU

Prevention and control

Now extinct due to immunisation
programmes. This was possible due to low
rates of mutation and therefore little
antigenic variation.

In addition, there was no animal reservoir.

Influenza https://www.youtube.com/watch?v=3n9L1-qJ36s

Name of pathogen
3 main sub-groups such as H1N1
Type of pathogen
Virus
Site of infection and symptoms
Upper respiratory tract causing a sore throat, coughing & fever.

Source and mode of transmission

Airborne droplets through coughing and sneezing of infected
individuals in close proximity.
Prevention and control
Quarantine & hygiene – difficult to control.

Annual vaccination programmes, but due to

high mutation rates forming new antigenic
types this is not always effective.

Treatment
Antibiotics are ineffective against influenza and are only used to treat the
symptoms of secondary bacterial infection.

Rest, keep warm, drink plenty of fluids and take painkillers.

Malaria https://youtu.be/8-qticNg5o

Name of pathogen
Plasmodium
Type of pathogen
Protoctistan
Site of infection and symptoms
Liver cells & red blood cells, causing them to burst when more parasites are
produced. Symptoms include severe bouts of fever and flu-like illness, headache,
muscle aches, and tiredness. Nausea, vomiting, and diarrhoea may also occur.
Source and mode of transmission
By a vector - a female mosquito from the genus Anopheles when feeding on
blood.
Prevention and control
Knowledge of life cycles. Nets, clothing
& repellent.
Vaccines difficult to develop.
Drug treatment to reduce the chances
of infection.

Treatment
Drugs that affect Plasmodium outside cells are
available but limited success and have side effects.
Malaria is caused by a single-celled parasite of the genus Plasmodium.
Malaria is endemic in some sub-tropical regions, and is caused by a single-celled parasite of the
genus Plasmodium. This parasite belongs to the kingdom protoctista. There are five different
species of plasmodium that may cause malaria, but Plasmodium falciparum causes the most
deaths and Plasmodium vivax is also a major killer. Plasmodium is transmitted by species of
mosquito from the genus Anopheles.
https://www.youtube.com/watch?v=Jt5u1lX9yZI
Transmission occurs when the infected mosquito pierces the skin of a human to take a
blood meal. Only the adult females are vectors of the plasmodium parasite as these feed
on human blood and so can transmit the parasite from human to human. The adult female
mosquito is the primary host but does not suffer from the presence of the parasites.
Humans may be considered the secondary host and do show symptoms of infection,
including: High fever, sweating, headache, nausea, vomiting,
anaemia (low red blood cell count), diarrhoea.

Q. Why are male mosquitos not vectors of the Plasmodium parasite?

Male mosquitoes feed on the nectar of plants. They do not
feed off human blood like females.
Task: Match the statements with the appropriate number from the diagram.
Plasmodium travels to, and then invades liver cells, where they mature. 2/3

The infected mosquito takes a blood meal and the plasmodium parasite
enters the blood stream. 1

If a female mosquito were then to feed on the blood of an infected

individual the Plasmodium parasites infect the mosquito, which act as a 5
vector to pass the disease onto another host.

Liver cells rupture and release plasmodium parasites. They then invade
red blood cells and multiply asexually. Red blood cells then also rupture, 4
releasing more plasmodium, which invade other red blood cells. The
rupture of red blood cells results in severe fever.

*You are not required to remember the names of life cycle stages*.
Prevention of malaria relies on knowledge of the life cycle of both the vector
(mosquito) and the parasite (Plasmodium).
Preventative measure Reason for effect Pyrethroid kills mosquitos
(the vectors)

Sleep under nets Mosquitos feed at night Larvae are aquatic: fish eat
them.
Nets are treated with the Pyrethroid kills mosquitos (the
pyrethroid insecticide vectors for plasmodium) After they mate with females
no offspring are produced.
Responding to mosquito Spray indoor walls with Kills mosquitos as they rest on
behaviour insecticide walls after feeding
Mosquitos feed at night.
Drain or cover stagnant Removes female mosquitos
water e.g. water tanks, ponds access to egg-laying sites
Removes female mosquitos
Prevents larvae piercing surface
Film of oil on the water to obtain oxygen access to egg laying sites.

Larvae are aquatic: fish eat Kills mosquitos as they rest

Fish introduced into water them on walls after feeding.
Infecting mosquitos with Bacteria infection blocks
Prevents larvae piercing
Biological control bacterium plasmodium development in the
mosquito surface to obtain oxygen.
Male mosquitos sterilised After they mate with females no
with offspring are produced Bacterial infection blocks
X-rays Plasmodium development in
the mosquito.
Drug treatment is available, but mainly to reduce the chance of
infection.

Q. Why do you think vaccines have proved difficult to develop?

The Plasmodium parasite has

high mutation rates and so
there are many antigenic types.
 RECAP – what was the Q?
1. There can be many different strains of a particular microorganism. Each with
slightly different antigens (proteins) on their surface, and each will trigger a
new immune response from the body.
2. A is when there is a rapid increase in a disease at within a particular area. B is
when there is a rapid increase in a disease that is worldwide and crosses
international boundaries.
3. Its granular cytoplasm contains lysosomes that can secrete digestive enzymes
to break down an engulfed pathogen.
4. Due to low rates of mutation and antigenic variation.
5. The lung neck & lymph nodes. Symptoms include coughing up blood and chest
pain.
6. Sleeping under nets treated with insecticide, infecting mosquitos and sterilising
male mosquitos with x-rays.
Immunology

Lesson objectives
• Describe the relationship between the pathogenic action of viruses
and their mode of reproduction.
• Describe the key features of antibiotics, including the mechanism of
action of penicillin and tetracycline.
• Understand how the overuse of antibiotics has resulted in the spread
of antibiotic resistant strains of bacteria.
 Virus reproduction

Viruses outside of the host cell are described as being inert. They are essentially particles
that can only replicate once inside a host cell, where the enzyme machinery of that host
cell is hijacked to make more viral copies. Viruses can be grouped into two main types of
reproduction cycle: the lysogenic cycle or the lytic cycle.

https://www.youtube.com/watch?v=7aEL0EQtyGA
Can you use the diagram to describe the
differences between the lytic and lysogenic cycles?
In the lytic cycle, viruses immediately reproduce using the hosts metabolism to copy
their nucleic acid and synthesise new coat protein (capsid).
Once new viral particles (virions) have been assembled in the host cell cytoplasm,
new viruses will leave the host cell (where they can then infect new cells) in one of
two ways:
• Lysis of the host cell e.g. common cold virus
• Budding from the host cell surface (where the virus becomes enclosed by part of
the host cell membrane) e.g. influenza virus
In the lysogenic cycle, following penetration of the host cell and shedding of the capsid, the
viral nucleic acid is integrated into the host cell genome and may remain there for many cell
generations with no clinical effect. They enter the lytic cycle at some time later, which is
when symptoms are produced e.g. Herpes simplex virus, HIV virus.
Thinker: What factors might cause the lysogenic cycle to become active
i.e. what factors might result in symptoms being seen in the herpes
virus?
Stressful conditions such as heat, toxic substances, lack of nutrients, etc.
 Starter
Lytic key points:
• Virus reproduces
immediately inside host
• New viruses leave cell (cell
• Can you draw a picture to represent the lytic
lysis)
cycle?
• Next can you draw a picture to represent the
Lysogenic key points:
lysogenic cycle? • Viral nucleic acid integrates
into host nucleic acid
• New host cells produced
Challenge: what disease does the HIV virus go same nucleic acid
have this
on to AIDS.
Challenge: form? Why can
Depends how welongnot predict
it takes for •exactly
May show lytic cycle after a
thewhen this will
viral nucleic acidhappen to an individual?
to be transcribed and while
translated for the lytic cycle to occur – depends
on stress factors.
Viruses can be pathogenic in a number of ways (causing death of the host cell):

1. Cell lysis: when viruses escape from cells to infect other cells/organisms
2. Production of toxic substances
3. Cell transformation: viral DNA can integrate into the host chromosome. If the DNA inserts
into a proto-oncogene or tumour suppressor gene it can result in the cell undergoing rapid
and uncontrolled cell-division i.e. becoming cancerous.
4. Immune suppression
• Viral DNA transcribed into mRNA
• And viral RNA
• mRNA codes for sequence of amino acids/has codons to code for
amino acids
• At ribosomes
• Viral proteins produced
• Viral protein and viral RNA combine to form a new virus/virion
Antibiotics
What are they?
You have two minutes to
answer these questions on a
board – by yourself! How are they
Then you are to swap with produced?

your partner and see if you

can add anything extra to
their answers .
What do they
affect?

Are there any

problems with
their use?
Gram positive bacteria

These lack the lipopolysaccharide

layer in their walls and but have a
thick peptidoglycan layer in
their cell wall. These bacteria are
affected by lysozyme and penicillin.
EG – Streptococcus. Staphylococcus.
Gram negative bacteria

More complex walls. Thinner cell wall

layer of peptidoglycan but contain an
additional lipopolysaccharide
membrane.
EG – Salmonella. Escherichia coli.
Antibiotics https://www.youtube.com/watch?v=X1GT2bKgci8
Definition:
A substance produced by a fungus which diminishes the population
Lysis
growth of bacteria
Lipopolysaccharide
Peptidoglycan
Types of antibiotics
1. Bacteriostatic – prevent the growth of bacteria Penicillin
2. Bactericidal – kill bacteria Red
Negative
Antibiotics are produced by fungi and act on bacteria, but not on eukaryotic cells or viruses. They can therefore treat
bacterial infection without harm to the patient.

Complete the blanks below describing bacterial cell wall structure:

peptidoglycan consisting of molecules of polysaccharide cross linked by amino acid side chains.
• Contains _________________
lysis
This provides strength and prevents osmotic __________.
• In some bacteria this cell wall is surrounded by an outer layer of lipopolysaccharide
________________.
negative and they retain a counter
• The gram stain reaction highlights cells with this additional layer (gram __________)
red
stain and appear pink/_____.
• The presence of this extra layer provides gran negative bacteria with protection from some antibacterial agents
penicillin
such as lysozyme and _______________.
Tetracycline - bacteriostatic

Tetracycline can prevent the growth of many different species of bacteria including Gram +ive
and some Gram –ive species. It acts as a competitive inhibitor of the second tRNA binding site
on the 30S subunit of the ribosomal subunit in bacteria.

What effect would this have?

• A tRNA molecule cannot bind
Site 1 (P site) Site 2 (A site)

mRNA at the second binding site

• Preventing a codon-anticodon
complex
Ribosome moves along mRNA
(towards 3’ end)
50S
• Adjacent amino acids won’t join by
peptide bonds 30S

• Translation and protein synthesis is

prevented.
Codon 3 Codon 4 Codon 5
Penicillin - bactericidal
Affects the formation of cross-linkages in the peptidoglycan cell wall during growth and
division of bacterial cells. It does this by inhibiting the enzyme responsible for the formation of
these cross-linkages (transpeptidase). Penicillin binds irreversibly to transpeptidase and it is
not complementary to the active site of this enzyme. The enzymes function is permanently
altered.

Using information from the text, explain what type of inhibitor penicillin is?
Penicillin is a non-competitive inhibitor as it has a shape that is
not complementary to the active site.
As a result the cell wall is weakened. What effect would this have if the cells were placed in
a hypotonic solution?
If there is a higher water potential outside the cells water will enter the
bacterial cell by osmosis. Eventually the cell will lyse (burst) as the
weakened cell wall is not strong enough.

Gram positive bacteria are more susceptible to penicillin due to their thick peptidoglycan cell
wall. Gram negative only have a thin peptidoglycan cell wall and contain the outer
lipopolysaccharide layer and so are penicillin is less effective against these bacteria.

Why are viruses not affected by antibiotics?

Viruses have no cell wall or metabolic pathways

(e.g. protein synthesis) to disrupt.
What problem might
arise due to overuse
of antibiotics?
Overuse of antibiotics
Antibiotics were used extensively in the Second world war
to save huge numbers of lives. Since then they have been
used extensively to treat infections in people, but also to
prevent infections in farmed animals.

There are two sources of antibiotic resistance alleles:

• Bacteria divide under optimum conditions and have a
high mutation rate. Naturally occurring mutations that
confer resistance to antibiotics have given these bacteria
a selective advantage in the presence of antibiotics
• Plasmids containing the antibiotic resistance allele can
be transferred from one bacterium to another via
conjugation.
 Overuse of antibiotics has resulted in the accidental selection of bacterial strains that are
completely unaffected by some antibiotics.

When does antibiotic resistance provide a selective advantage to a bacterium?

When they are in the presence of the antibiotic
Is it always an advantage?
No. If the antibiotic is not present then the resistant bacteria have no advantage over
non-resistant bacteria.
Why does overuse of antibiotics cause problems therefore?
Using antibiotics provides resistant bacteria with a selective advantage. Non-
resistant strains die and only resistant ones are left to reproduce. This will result in
a fully resistant population forming.
MRSA
Antibiotic disc practical set up

• You have been provided with a nutrient agar plate that has a bacterial culture
growing on it. You need to add an antibiotic disc to your plate.

• Can you predict what will happen to the bacteria growing on the plate?

• What might your culture look like after it’s been in the incubator with the
antibiotics for 2 days? Draw this…
Antibiotic disc practical results
• Measure all of your clear zones. What is your mean, median, mode? (see
below for help if unsure)
• Work out the area of your two largest clear zones – πr2
• Which antibiotic has worked the best? How do you know this?
EXT: a sample of bacteria was taken from 2 zones of inhibition and cultured on
nutrient agar. The following results were found after incubation. Conclude the
mode of action for each of these antibiotics and explain your answer.
Mean – the sum of all values divided by the number of
a b values
Median – the middle value. If there is an odd number of
values it is just the middle one. if there’s an even number
it’s the mean of the middle two.
Mode – the value which occurs most often in the data
set.
RECAP
• Write 9 key words onto a white board from the booklet so far (not the
first page)
• When I read out a definition – if you know what I’m describing shout
the word out.
• Lets see who gets all 9 first!
 Immunology

Lesson objectives
• Understand how natural barriers reduce the risk of infection
• Distinguish the innate from the adaptive immune system
• Describe the primary and secondary immune responses
List…

• As many ways in which our body defends against pathogens (2mins)

o When you’re done read them out to your partner
o Any you both have cross out
o The person with the most unique answers wins!

Now cut and stick the

appropriate description next
to the headings in your
booklet…
Passive Immune Response - INNATE
Blood clotting:
Inhaled air: If capillaries are broken, blood clots
prevent the entry of pathogens.
In the trachea mucus traps
microorganisms and cilia waft to bring
the mucus up and out of the trachea. Tear ducts, saliva and stomach:
Lysozyme in tears and saliva hydrolyse
(note: cilia in the nose filter air and trap peptidoglycan cell walls to kill bacteria.
dust particles but they don’t waft and Stomach acid kills many bacteria.
no mucus is produced).

Phagocytosis:
A phagocyte engulfs a bacterium,
Skin: enclosing it in a vacuole. Lysosomes fuse
Covers the external surface of the body. with this vacuole releasing hydrolytic
Vitamin C is required to maintain strong enzymes that digest the bacteria.
connective tissue. Skin flora:
Bacteria and fungi found on our skin offer competition for
pathogenic bacteria. These natural flora don’t wash off the
body as easily as pathogenic bacteria.
 RECAP – true or false? *If false correct it!
1. Gram negative bacteria have a thin peptidoglycan cell wall and a protective outer lipopolysaccharide
layer TRUE!
2. Bacteriostatic antibiotics kill bacteria by causing cell lysis FALSE! Bacteriostatic prevent the growth
3. Tetracycline is an example of a bacteriostatic antibiotic, it binds to the second tRNA binding site on an
80s ribosome, preventing protein synthesis. FALSE! A 70s ribosome
4. Penicillin is an example of a bactericidal antibiotic. It prevents bacterial cell wall formation and so the
cells lyse due to a weakened cell wall. TRUE!
FALSE! Only when in the presence of the antibiotic
5. Bacteria with antibiotic resistance alleles have a selective advantage over other bacteria at all times
6. Goblet cells produce mucus to trap microorganisms and our cilia waft to remove this from our body TRUE!
7. Lysozyme in tears kills all bacteria FALSE! Gram positive
FALSE! Vitamin C
8. Our skin covers the surface of our body and vitamin K is needed to maintain strong connective tissue
9. Phagocytes are agranulocytes that engulf pathogens so that lysosomes can release digestive enzymes to
hydrolyse the pathogen FALSE! Granulocytes
10. Our blood clots to prevent the entry of pathogens if our vessels become broken TRUE!
EXT: our passive immune response is also known as our adaptive immune system. FALSE! Innate immune system
 But what happens if pathogens make it past these barriers and into our
bodies?

Specific immune response - ADAPTIVE

In the adaptive immune response the body produces a specific response to a foreign antigen.

Lymphocytes provide this response.

What are lymphocytes?

Type of leucocyte (agranulocytes).

There are two components to the adaptive immune response:

1. The humoral response

Results in the production of
antibodies

2. The cell mediated response.

Refers to the activation of
phagocytic cells, B-lymphocytes
and T-lymphocytes.
The humoral response
• B lymphocytes are produced in the bone marrow and activated in the blood, spleen and lymph nodes.
• Millions of different B cells circulate in the blood stream and lymph vessel. Each has specific receptor on its
surface which bind to one type of antigen.

Can you use the diagram to describe

what happens when…
• A foreign antigen enters the
blood or lymph vessels and a
specific B lymphocyte binds to it

• When this foreign antigen ever

enters the blood or lymph nodes
again in the future
When foreign antigen enters the blood or lymph vessels specific B cells bind to the foreign antigens. The B
cells become activated and they undergo clonal expansion to produce:
• Plasma cells: which secrete antibodies specific to the foreign antigen which activated the B cell
• Memory B cells: which remain dormant in the blood, spleen and lymph nodes and then divide to form
more B lymphocytes if the same antigen is encountered in the future.

Clonal expansion
 Antigen B cells
Pathogen
B lymphocyte with a complementary
receptor binds to pathogen Remain dormant in the
lymph system and then
divide
Memory B cells in the future to form
more B lymphocytes if the
same
antigen is encountered in
the future. (faster
response)

Secrete antibodies
These cloned cells
The activated B lymphocyte divides to
then
formdifferentiate
clones (clonal expansion)

Plasma cells
HW booklet Q
Antibodies
• Antibodies are Y shaped globular proteins (immunoglobulins, often given the symbol Ig).
Each antibody molecule is made from four polypeptide chains and has two antigen binding
sites.
• Each antibody is specific to the antigen to which they bind, forming an antigen-antibody
complex.
• When antibodies bind to the antigen and form an antigen-antibody complex, they render the
antigen inactive. Such as through agglutination (the clumping together of bacteria). This
allows phagocytes to locate and engulf the pathogens.
 The tips of the Y structure
specific and complementary to
a particular shape of antigen –
antigen binding sites.

light Variable
light
chain region
chain

Disulphide
bridges
Constant
regions
heavy heavy
chain chain
Plasma cell

Agglutination
 Remote Learning
• I will be working through theory just as we would in the classroom. We will complete some activities
alongside the theory and may complete / mark exam Qs if we have time.
• Please ensure you have with you:
• Theory booklet Please join pear deck:
• Exam Q booklet
• Whiteboard & pen joinpd.com – code: ajqbco
• If you don’t have the resources they can be found on SharePoint under 01. remote learning – UVI.
• If you can’t access or print these right now please make notes on paper and these can be copied up once
you get the physical booklet.

• If you have any Qs please write these down and ask them in the teams chat or write them in peardeck
(joinpd.com – code: ajqbco). I will answer these at the end of the session.

Chat soon 
 What’s the highest level of protein structure an antibody has?
Quaternary

What type of bond (covalent) holds the polypeptide chains together between sulphur containing variable
groups?
Disulphide bonds/bridges

Explain how the structure of an antibody ensures it only binds to one type of antigen?
The variable region is specific and so the antigen binding site is only complementary to one type of antigen

In agglutination microbes are clumped together. This allows them to be destroyed (e.g by phagocytosis) more
efficiently, How is the structure of an antibody adapted to help agglutination occur?

As there are two antigen binding sites so the antibody can bind to two antigen molecules (two pathogens) at once
Humoral response
A B lymphocyte binds to a specific antigen. This stimulates the B lymphocyte
to undergo clonal expansion (mitosis).
After differentiation, two types of B lymphocyte are formed:
• Plasma cells – these secrete antibodies specific to the antigen. Antibodies
bind to the antigen and hold the pathogen in place. Phagocytes can then
come and engulf the pathogens, allowing hydrolytic enzymes to digest and
kill the pathogen.
• Memory cells – these remain dormant in the blood. If the same antigen is
even encountered in the future, the memory cells will divide by clonal
expansion to produce plasma cells. This will allow for the rapid production
of antibodies.

https://www.youtube.com/watch?v=2DFN4IBZ3rI
 Summary
• Use the craft materials to summarise
the humoral response.
• Ensure your model is annotated.

Extension: HW Q 7e
Helper: a null hypothesis states there is
no significant difference. If the value is
less than the value at the 0.05
significance we accept the null
hypothesis.
Starter Whiteboards

Task: Draw the antibody shown, name 1-7 and answer the questions at the bottom

6 region
Variable
light chain
1 1
light 2
chain
2 Constant7 region
Disulphide bonds/bridges The “tips” of the Y shaped
5
antibody bind to an epitope on
both bacteria causing them to
heavy4chain 2 together
clump
heavy chain 1
3

Questions: Extension:
• Circle parts of the antibody that are complementary in shape to the antigen • What is agglutination
on the surface of the pathogen • Draw a diagram to show
• What type of lymphocyte secretes antibodies? agglutination involving 2
• What level of protein structure does an antibody have? bacteria
Remember - There are two components to the adaptive immune
response:

1. The humoral response

Results in the production of
antibodies

2. The cell mediated response.

Refers to the activation of
phagocytic cells, B-lymphocytes
and T-lymphocytes.
 Cell mediated response
Phagocytic cells take in pathogens such as bacteria by endocytosis.
pathogen
TASK - describe what is happening at
the three stages?
A lysosome fuses with the phagocytic vesicle
and releases hydrolytic enzymes to digest
the pathogen.

The phagocyte then displays a small part of

the pathogen (antigen) on its surface. 3

It is now called an antigen presenting cell

(APC).
The cell mediated response
T-lymphocytes originate from stem cells in the bone marrow, but are activated in the thymus
gland.

When phagocytes engulf a pathogen, the pathogen is hydrolysed into component parts. The
phagocyte can then present some of these parts (antigens) on it’s membrane surface. This
phagocyte is now an antigen presenting cell.
Other examples of antigen presenting cells include:-

• B lymphocytes

• Infected body cells

Antigen Presenting Cells

Normal cells Phagocytes B cells

infected with
a virus
When a T lymphocyte detects a T cell
specific antigen on an antigen
presenting cell, it is stimulated to Clonal expansion
undergo clonal expansion.
T helper cell Cytotoxic
(killer) T cell
T memory cell

Produce chemicals called Remain dormant in the Kill infected body

cytokines which: circulation and then cells (that have
1. Stimulate more divide to form more T specific antigens on
https://www.youtube.com/wat phagocytic cells to lymphocytes if the their surface) by
ch?v=jgJKaP0Sj5U migrate to the infected same antigen is lysing the cells. E.g a
tissue, which then engulf encountered in the normal body cell
more of the pathogens future. infected by a virus.
and digest them;
2. Stimulate clonal
expansion of plasma B
cells to make and secrete
antibodies specific to that
particular antigen.
Cytokines – produced by T helper cells

1. Stimulate more phagocytic cells to

migrate to the infected tissue, which
then engulf more of the pathogens
and digest them;

2. Stimulate clonal expansion. This is

rapid division of B cells means large
concentrations of antibodies are
produced.
Cell mediated response
A T lymphocyte binds to an antigen presenting cell. This could be a
phagocyte, B lymphocyte or an infected body cell.
This stimulates the T lymphocyte to undergo clonal expansion (mitosis).
After differentiation, three types of T lymphocyte are formed:
• Helper cells – these secrete chemicals called cytokines. These stimulate the
clonal expansion of B lymphocytes. They also stimulate phagocytes to come
to the infected area.
• Cytotoxic cells – these kill infected body cells by rupturing the cell
membrane and causing lysis.
• Memory cells – these remain dormant in the blood. If the same antigen is
even encountered in the future, the memory cells will divide by clonal
expansion to produce more T cells.
https://www.youtube.com/watch?v=rd2cf5hValM
Summary
• Use the craft materials to summarise
the cell mediated response.
• Ensure your model is annotated.
 Whiteboards
Task: True or False?
State if the following statements are true or false. If they are false you need to justify your
choice by correcting the sentence

1. The innate immune response is non-specific and the first line of defence
2. The cell-mediated immune response is part of innate immunity
3. The humoral response is one part of adaptive immunity
4. The humoral response involves secretion of antibodies from Plasma B cells
5. Antibodies are globular proteins with an overall tertiary structure
6. Both phagocytes and B lymphocytes can be antigen presenting cells
7. T helper lymphocytes recognise specific antigen and secrete cytokines
8. T helper lymphocytes can directly kill the cell they are attached to
 Lymphocytes
Phagocytes

T cells

Secrete large
B memory
concentrations of
cells
antibodies T helper
cells

B memory cells
These bind to cells presenting
T cells the complementary antigen
Phagocytes (macrophages) and kill them e.g. causing cell
Lymphocytes lysis.
T helper cells
 Whiteboards

Task: complete the following maths questions

1. A B-lymphocyte became activated and divided by clonal expansion and formed 34 clonal cells. 28 of these
clonal cells then differentiated into plasma B cells and the remainder formed memory B cells. What percentage
of the original clonal cells formed memory cells?
(6/34) x 100 = 17.6 %
2. If each of these memory B cells recognised the specific antigen again on re-exposure to the pathogen 6 months
later, they would undergo clonal expansion. From the clones that are made, 80 became new memory B cells.
What percentage increase is this from the original memory B cells?

(80 – 6)/6 x 100 = 1233 %

Extension:
If there were 12 lymphocytes in one mm3 of blood, how many lymphocytes would there be in one cm3 (hint:
be careful, this is a volume conversion)?

12,000 cells
TASK
1. Watch the video on primary and secondary immune response
2. Try and fill out the blanks on page 20 using your current knowledge,
knowledge gained from the video and information in the graph
3. Use the word bank below to help if you’re struggling

Concentrated, symptoms, agglutination, cytokines, latent x 2,

plasma x 2, membrane, engulf, clonal, antibodies, infected

https://www.youtube.com/watch?v=b9CLL8idzf8
 Primary immune response
SECONDARY RESPONSE

concentration in the
Short latent

Antibody
PRIMARY

blood
RESPONSE period

Latent
period

First exposure Second exposure

Time

• On first exposure to the antigen, there is a _________

latent period .
engulf
• Phagocytes __________ the foreign antigen/cell/virus.
membrane B cells and ___________
• The phagocyte incorporates part of the antigen on its own cell __________, infected body
cells also present antigens.
clonal expansion to form helper T
• These antigen presenting cells activate specific T cells which undergo __________
cytokines
cells which release ___________.
• Cytokines stimulate B cells to undergo clonal expansion forming many __________plasma B cells which start
antibodies against the antigen. Memory cells are also produced.
secreting ___________
agglutination
• Antibodies are specific to the antigen and bind, holding the pathogen in place (______________).
• The B plasma cells secrete a low level of antibodies for about 3 weeks, after which the infection usually
subsides (this time period can vary).
Secondary immune response
SECONDARY RESPONSE

concentration in the
Short latent

Antibody
PRIMARY

blood
RESPONSE period

Latent
period

First exposure Second exposure

Time

Explain why the latency period is much shorter and the antibody
production much greater in the secondary immune response.
latent
• On re-exposure to the same antigen, after a very short _________ period, memory cells undergo
rapid clonal expansion.
plasma
• A small amount of antigen stimulates rapid production of __________ B cells.
concentrated
• Antibodies are made much more quickly and more ______________ than in the primary
response.
symptoms develop.
• The antibodies remain at high concentrations for longer and no _________
 Immunology

Lesson objectives
• Distinguish active from passive immunity
• Describe the differential effectiveness of vaccines
• Consider the ethics behind vaccination programmes
Can you describe the differences between passive and
active immunity?
Passive immunity
In passive immunity the body may receive antibodies that have been produced by another
individual. Protection is short lived because the antibodies are recognised as non-self and are
destroyed and no memory cells are produced. Examples include:

• Natural when antibodies are transferred to the foetus via the placenta, or to the baby in
breast milk.
• Artificial when pre-synthesised antibody is injected into an individual e.g. tetanus antitoxin
Active immunity
In active immunity the individual produces their own antibodies. Protection is
long-lasting due to the production of antigen-specific memory cells. Examples
include:

• Natural production following infection

• Artificial production following vaccination e.g. against Rubella.
Complete the summary table below on P21

Antibodies? Memory cells Artificial

produced? Examples
Active Produced by the individuals immune Yes - B and T Vaccination e.g.
immunity system. memory cells Rubella
Natural – infection formed
Artificial – vaccination

Passive Antibodies received have been No Tetanus

immunity produced by another individual. antibody
Natural – foetus through the placenta, injection
baby via breast milk
Artificial – antibody injections
Antibody injections
In an emergency, antibodies can be injected to provide rapid protection against a
pathogen, e.g. in cases of rabies. This allows time for a persons immune system to
develop an active immune response. Injections of antibodies are also used with people
who do not develop a strong immune response to a vaccination or who have a
weakened immune system.
How many vaccinations have you had?

What for?

Vaccines can be:

Weakened versions of the pathogen

1. ……………………………………………………………………………………………………….
Antigens isolated from the pathogen
2. ………………………………………………………………………………………………………
Inactivated toxin
3. ………………………………………………………………………………………………………
Inactive or killed pathogen
4. ………………………………………………………………………………………………………
 How do vaccines weakened
Often, a ___________ or inactive form of the pathogen is injected into an individual.
work? Complete the
timeline on page 20 Specific antigens on the pathogen will be detected by specific B and T
of your booklet… lymphocytes
__________________.

clonal
B and T cells will undergo ___________ expansion, triggering an immune response.

symptoms
The individual may show some _____________ as their body will undergo a normal
immune response to the weakened pathogen.

memory
As part of this response, ______________ cells will be produced.

Successful vaccines must be:

• Safe (no/little side effects) If the same antigen is ever encountered in the future, memory cells will undergo
• Effective (trigger an immune response) clonal
rapid ____________ expansion.

symptoms
The pathogen will be destroyed before it can produce any _____________, so the
immune
person is said to be _______________.
How effective are vaccination programmes?
Pathogens that exhibit no or low levels of antigenic variation (e.g. Rubella) are more likely
to be protected by a single round of immunisations.

Pathogens that have many antigenic types and mutate frequently are more difficult to
protect against (e.g. Influenza). Protection against these organisms require repeated
immunisation against the most common antigens, however even this isn’t always
effective.

In the UK, some individuals are offered flu vaccinations on the NHS. What types of
individuals would this be?

Older / immunocompromised/ asthmatic people.

How often are they offered these injections? Why?
Annually – there are many antigenic types of influenza and new types are always
occurring due to high mutation rates. Annual vaccinations contain a few strains that are
predicted to be the most prevalent that year.
Herd immunity
• If enough people in a population are
vaccinated the spread of disease is controlled
so even people who are not vaccinated have
some protection.
• Herd immunity relies on a certain proportion
of the population being vaccinated. If
number of people vaccinated falls below a
critical level, disease may be able to spread.
DEBATE: Ethical considerations.
In pairs: one of you must come up with at least 2 arguments for vaccinations,
the other must come up with at least 2 arguments against them.
The rights of the individual when
Cost v’s effectiveness of
considering mandatory compared to
the vaccine.
voluntary programmes.

Ethics
Protection of the individual
Side effects, whether real compared to the protection of
or perceived. the community.
HW
• Complete immunology EXAM Qs
• Complete immunology myLoreto QUIZ

• Peardeck – joinpd.com – pvq irt

M1.(a) (i) 1. (Scientists) cant show bias / influence / may have a vested
interest / work for the company developing the vaccine;
Relates to the scientists
2. (Volunteers) can’t show psychological / mental effects / ‘placebo effect’ / expectations;
Relates to the volunteers
Neutral: so they have no idea what they are taking
2
(ii) Any two suitable suggestions, eg
Neutral: refs. to age and health
1. Amount of nicotine in cigarettes;
Neutral: different types of cigarette / different ways / frequency of smoking
2. Amount inhaled / absorbed / time since last cigarette;
Neutral: absorption by gut / digestion
Accept: absorption by mouth
3. (Different) amounts excreted / metabolism / rate of binding (of nicotine) to protein;
Accept: broken down (differently)
4. (Different) blood volumes;
Neutral: different body masses
5. Nicotine from passive smoking / other smokers / other sources;
6. Some volunteers received the vaccine / placebo;
Accept: some volunteers would have / would not have the antibodies
2 max
(b) (i) 1. Antibodies to nicotine produced /
antibodies bind to nicotine;
Q Reject: vaccine contains / produces antibodies
Q Neutral: antibodies digest / kill / fight nicotine
2. (So) nicotine does not bind to protein / does not
reach the brain;
Q Reject: any reference to ‘active site’
Neutral: idea that the antibodies bind to the protein
3. (So) cigarettes / smoking does not satisfy
addiction / reward smokers / release (reward)
chemicals;
3
c) A journalist reported that this vaccine is a major
breakthrough in helping people to stop smoking. Do these
data support this statement? Explain your answer.
(c) 1. High antibody responders have a high % to stop smoking / are more likely to stop smoking;
‘People producing a high concentration of antibodies’ is equivalent to ‘high antibody responders’
Accept: reference to values from the table
2. Only a few may be high antibody responders / no numbers on how many are high / medium / low
antibody responders;
Neutral: not all people are high antibody responders
3. Percentage who stopped smoking is similar for placebo group and low / medium responders / some / %
of placebo group (still) stopped smoking / placebo has the lowest value / % to stop smoking;
Accept: reference to values from the table
4. Large sample size / double blind so reliable / representative;
5. Antibody levels peak at / drop after 5 months / boosters may be needed at / after 5 months;
6. May start smoking again after 5 / 6 months / do not know the percentage who stopped smoking after 5 / 6
months;
7. Nicotine is not the only factor responsible for making people smoke;
Must mention nicotine
Do not accept: correlation does not mean causation / could be due to other factors
5 max
Exam Questions
Extension: Influenza (virus)
There are three sub-groups of the influenza virus: FluA, FluB
and FluC. FluA is the best known and will be described here.
These influenza viruses infect not only humans, but many other
species including pigs and birds. Avian (bird) flu virus and
RNA polymerase:
Swine (pig) flu viruses haveOnce alsoinsideled to cellformation
the host this of new
viral enzyme helps make the Haemagglutinin (H):
viruses that can infect humans, which
+ strand often
of viral mRNAlead
that to pandemics. Surface protein which
has a role in virus
This is described in detail laterbinds
on to (see: Antigenic
host cell ribosomes shift).
entry into host cell

When a new strain of influenza virus appears in humans

(where the new virus has new proteins on it’s surface different
to the original virus), the human immune
Neuramidase (N): system is not able to
provide adequate protection Surface
straight away.
protein which The body will need
has a role in virus exit Phospholipid bilayer:
to start making antibodies against
from hostthe
cell new virus, which is why
Derived from the host
infection can set in before this new virus is cell’s membrane as the
virus exits the host

RNA:
There are 8 RNA molecules (called – strands).
These need converting into complementary +
RNA inside the host cell which are then each
translated to make new viral proteins
Summary notes:
• Influenza virions are retroviruses
• Outer phospholipid envelope is from the host cell
• protein ‘spikes’ (glycoproteins) called H and N project from the envelope
• H and N determine the subtype of influenza virus (e.g. A: H1N1)
• Antibodies made by humans that bind these spikes may protect us against infection
• The viral protein M1 forms a shell giving strength/rigidity to the phospholipid
envelope
• Inside the virion are 8 viral RNA strands. These are the genetic material of the virus
• Each RNA strand is joined with a viral RNA polymerase enzyme
• The 8 RNA strands code for different viral proteins (that will later assemble in the
host cell)
The influenza virus attacks the mucous membranes, especially in the upper respiratory tract, often causing sore throat,
coughs and fevers. Spread of the virus is not easy to control, as it may easily be inhaled in droplets from coughs and sneezes
(aerosol transmission). It also survives better when the air is dry and there is low ultra-violet light in the environment.
Mucous in the respiratory tract also protects the virus.
Using this information, why might the flu be more common in winter than in summer?
In winter there is drier air and lower levels of ultra-violet radiation.

How might you reduce the risk of influenza virus transmission?

Regular and thorough handwashing
Using and discarding tissues for coughs and sneezes
Annual vaccinations
There are many antigenic types of influenza virus. The different types have two origins:
1. Antigenic drift
Antigenic drift refers to gradual changes to the influenza virus that happen slowly over time due to mutations in the
viral RNA. This results in different versions of virus particles which cannot be inhibited as effectively by the antibodies
that were originally targeted against previous virus strains, making it easier for the virus to spread throughout a
partially immune population. This causes changes to the seasonal influenza that requires us to get new vaccine against
that flu strain each year.

What viral proteins (antigens) tend to get altered by mutations?

The viral genes for H and N tend to get mutated, making these proteins (antigens) on the surface of the new
virus different.

How do these mutations in the viral RNA occur?

When the new viral RNA is made, some mutations are introduced because viral RNA polymerase has no proof-
reading ability.
2.Antigenic shift
Antigenic shift is the process by which two different influenza viruses combine to form a new influenza virus having a
mixture of the surface antigens of the two original strains. Antigenic shift occurs only in influenza virus A because it infects
more than just humans (e.g. chickens, pigs, whales, horses, and seals).
Influenza strains are named after their types of hemagglutinin (H) and neuraminidase (N) surface proteins, so they will be
called for example H3N2 for type-3 hemagglutinin and type-2 neuraminidase. Each virus has one type of H and one type of
N protein.
How does Antigenic shift occur inside the host cell after infection?

When two different strains of influenza A virus infect the same host cell simultaneously, their lipid envelopes and protein
capsids are first removed exposing their RNA which is then transcribed to mRNA in the host cell cytoplasm. The host cell then
forms new viruses that may contain RNA from both of the original viruses; for example, if H3N2 and H5N1 infect the same
host cell, a new virus H5N2 may form this way. Because the human immune system has difficulty recognizing this new
influenza strain, it may be highly dangerous and result in a new epidemic or even pandemic (i.e. if humans have no circulating
antibodies specifically against the new virus it can spread rapidly).
Avian influenza A (strain = H3N8) Please note:
• Contains 8 RNA strands/genes
The host cell in this example of antigenic shift is in pigs
• One RNA strand codes for H3
• One RNA strand codes for N8 Host cell = Pig (swine) epithelial cell
Infected by H2N2 + H3N8 simultaneously
Some new virions formed containing H3 + N2 RNA

Human influenza A (strain = H3N2)

Can also
infect • Contains 8 RNA strands/genes
• One RNA strand codes for H3
• One RNA strand codes for N2

Human influenza A (strain = H2N2)

• Contains 8 RNA strands/genes
• One RNA strand codes for H2
• One RNA strand codes for N2

New virus that can

Can also infect human cells
infect (pandemic strain)
Host cell (in pig)
25