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Describe the structure of the cell wall in the bacterium described above.

thick peptidoglycan cell wall
a polymer of modified sugars cross linked by short peptides.
Suggest the advantages of forming endospores. [1]
start to grow again when the environment is suitable

During B cell maturation:

Somatic recombination of VDJC/VJC gene segments occur to produce B cells with antigen receptors of different
Clonal selection
B cells with antigen receptors complementary to epitopes of bodys own molecules are removed by apoptosis

During primary immune response,

Somatic recombination of the VDJC/VJC gene segments
- occurs during development of a B lymphocyte Advantages:
- via removal of intervening DNA sequences gives rise to antibody diversity
- followed by ligation of gene segments
- by enzymes to respond to large diversity of molecular
At variable regions of Ig heavy chain gene locus: structures associated with pathogens
rearrangement of D and J gene segments
When asked for how SR give rise to Ig diversity:
followed by rearrangement of V gene segments
diff segments of V, D, J ligated to form genes
VDJ exon joined to the constant segments encoding diff variable regions in heavy chains
Only 1 segment from each is chosen
At variable regions of immunoglobulin light chain gene
locus Remaining gene segments removed
rearrangement of V and J gene segments Ref to no. of gene segments in context of qn
--> diff mRNA seq
VJ exons joined to the c segments
--> diff amino acid seq
during RNA splicing
--> diff specific 3D conformation of variable
Clonal selection
B cells with antigen receptors complementary in shape to the antigen selected
During clonal expansion of B cells,
occurs via mitosis to produce genetically identical daughter cells
results in increased production of antibodies
which can binds to complementary/ specific antigen present
to mediate increased rate of phagocytosis/ faster response during secondary infection
Somatic hypermutation: Class switching
1) in variable region of immunoglobulin chains 1) one constant region gene segment from IgM is
2) point mutations in rearranged VDJ gene segments replaced with another different constant region
3) occurs at higher rates than normal gene segment from IgG
4) produces B cells with membrane Ig having altered 2) gene segment coding for constant region of
antigen-binding sites IgG is ligated with other exons
3) occurs during somatic recombination in
Significance: activated B cells
Produces B cells with higher affinity B cell receptors which
will survive, proliferate and mature into plasma cells; Advantages:
results in different class of antibodies
So antibodies are generated with increasingly higher
affinity for antigen during an immune response; with the same antigen specificity

allowing for variable effector functions

Provides progressively better protection against pathogen
(affinity maturation)

Explain how vaccination can control disease.

-form of artificial active immunity ; uses weakened form of the disease causing pathogen
-stimulates immune response to destroy the attenuated version
-develops immunological memory [elicit more rapid, effective 2ndary immune response during subseq encounters]
-confers lifelong immunity [attenuated virus can replicate in host cells & not degrade in body -> no need for booster
shots to revive immunity in individuals]
First injection:
1) there is a lag phase
Time needed for:
1) Antigen presentation 2) Activation of T helper cells 3)Clonal selection, expansion/mitosis
4) Differentiation of B cells into plasma cells 5) prod. enough antibodies to fight infection
2) stimulates a primary immune response to produce antigen-specific memory B cells and
plasma cells, where only a small amount of antibodies are produced.
3) mainly lgM antibodies are secreted with low potency
Second injection:
1) stimulates secondary immune response, where many memory B cells (from primary
response) will be activated
2) to divide and differentiate into many plasma cells more rapidly and potently
3) that produces larger amount of antibodies
4) of different classes, due to class switching that has started in primary response
5) together with somatic hypermutation and affinity maturation, will produce plasma cells that
secrete antibodies with higher specificity and affinity for natural virus pathogen
How primary immune response is triggered:Prayers, To A Really Boring Animal, Seriously Allow Dire Problems, Please Memorise!
The vaccine contains inactivated toxin that acts as antigens
which is taken up by macrophage (APC) by Phagocytosis
which travels to secondary Lymphoid organs that contains mature naive T and B cells
The processed antigens are Presented by macrophages on MHCII glycoproteins on CSM
which is recognised and Bound by TCR of CD4+ T cells
which is then activated and proliferate by Mitosis
Activated T helper cells secrete Cytokines which activate naive B cells to Differentiate and Proliferate into plasma
cells and memory B cells.
Plasma cells produce Antibodies specific to and bind to pathogen quickly and effectively.
Memory B and T cells formed give Long-term immunity to pathogens
Infected cells will present the processed antigens to the CD8+ T cell via MHC I glycoproteins (A)
CD8+ T cells binds to antigen displayed by infected cells to differentiate into cytotoxic T cells (GBA)
Cytotoxic T cells then secrete Perforin that forms pores in the membrane of the infected cell.
Granzymes activate enzymes that trigger apoptosis, while Granulysin forms pores in the CSM, leading to osmotic
lysis of cell.
RNA viruses have high rate of mutation :
lack of proof reading capacity of virus RNA polymerase or RTase of retroviruses
errors in genome by virus RNA-dependent RNA polymerase not corrected
missense mutations result in in codon in mRNA
in 1 structure of virus proteins, including virus surface proteins
structural in viral surface glycoproteins that act as antigens
altered 1 structure leads to altered folding into 3 structure with alteration of 3D shape
in epitope no longer recognised by antigen binding site of antibody raised immune response to
constant mutations in virus surface proteins lead to continuous in epitopes
antibody raised in immune response to vaccine now have antigen binding site that is specific to the original
epitope can no longer bind altered epitope
unable to eliminate new strains of RNA virus that evolve from the original strain, so loss of immunity
Describe how the antibody is folded from linear polypeptide chains. [4]
1) hydrogen bonds between CO and NH groups along the polypeptide backbone;
2) give rise to a-helix and B-pleated sheets
3) interactions between R groups of amino acid residues
4) bends the secondary structure into tertiary/ globular shape
5) (quaternary structure) consist of 4 polypeptide chains
6) 2 heavy chains and 2 light chains

Explain why the type of immunity gained by G is described as passive immunity. [2]
1. No immune response elicited (no memory B cells produced)
2. Antibodies not made/ come from other sources
3. High concentration/ figure from graph, immediately/after injection/ on Day 0-1
4. Antibody concentration fall
5. Does not last long/ only approximately 2 weeks/ temporary

Explain why person H is considered to be better protected against future exposure to the tetanus toxin compared to
person G.
1. Person H has immunological memory (has memory B cells in circulation)
2. able to elicit a secondary response
3. which is rapid (by mitosis, clonal expansion)
4. and leads to larger production of antibodies (binds to specific antigens )

Explain why the vaccine is not effective for people aged 46 and above. [2]
1. As people age, the thymus shrinks
2. repertoire of naive T cells will be lower
3. Activation of T cells and B cells by the vaccine will be lower
4. unable to form memory T cells and B cells.

First line/ barrier defences Second line/ Cellular Innate Defences

Physical: e.g. skin and mucus Complement proteins are activated:
Prevent entry of pathogen Formation of pores (through membrane attack complex--> cell lysis);
Enhanced phagocytic activity of macrophages
Chemical: e.g. lysozymes in Cytokine and histamine secretion:
tears; hydrochloric acid in Stimulates recruitment of macrophages, neutrophils
stomach resulting in inflammation (dilation of blood vessels), causing pain
Destroy cell walls of Pyrogen secreted by activated macrophages
susceptible bacteria; increases temperature, causing fever
low pH denatures enzymes in
pathogen Importance: respond immediately to invasion from pathogens to contain and get rid
of the infection

State how a B cell is able to produce IgM and IgD at the same time. [1]
- Alternative splicing of the pre-mRNA.

Explain what is meant by mutation, and outline its advantages and disadvantages to animals. [13]
Explain what is meant by mutation
1. inherited change in nucleotide sequence
2. base-pair insertion, deletion and substitution
3. changes to chromosome structure and number
Single Gene Disorder
1. sickle cell anaemia
2. base-pair substitution (CTT--> CAT GAA --> GUA)
3. in B-globin gene
4. reduced ability to carry oxygen (Glu --> Val) --> block vessels, cell death if no O2 --> respiration
Multi Gene Disorder
1. accumulation of several diff mutations in a single cell lineage
2. lead to the development of cancer
3. gain of function of proto-oncogenes to oncogene
4. loss-of-function mutation in tumour suppressor genes
5. dysregulation of cell cycle checkpoints/ uncontrolled cell division
Chromosomal mutations
1. non-disjunction of chromosomes
2. during meiosis
3. leads to aneuploidy/ polyploidy
4. gives rise to a named genetic disease (Klinefetler (XXY), Down's syndrome) physical abnormalities,
impaired cognitive abilities
Evolutionary significance
1. raw materials for evolution (by increasing genetic variation)
2. give rise to phenotypic variation
3. allows natural selection to take place (select for different phenotypes)
4. increase chance of survival of species
5. lead to microevolution/ speciation
Increased affinity of antibodies
1. mutations in VDJ/ VJ regions (variable regions)
2. B lymphocytes produce antibodies with higher affinity
3. leading to affinity maturation
4. more effective immune response

Describe how TB is transmitted. [2]

M. tuberculosis
in droplet nuclei
enters the upper respiratory tract
and reaches the aveoli of the lungs

Ref to fig and your own knowledge, describe the formation of granulomas in M. tuberculosis infections. [3]
M. tuberculosis ingested by aveolar macrophages
replicate intracellularly
destroy aveolar macrophages
infect more macrophages
leads to activation of T cells
which surround infected macrophages
forming a barrier shell

Suggest how persistence of M. tuberculosis within granuloma allows it to replicate intracellularly. [2]
foamy macrophages provide lipids
for the formation of new mycolic acids

With reference to figure, explain why administering pencillin will not effectively treat TB. [2]
Penicillin only interferes with the interpeptide linking of peptidoglycan
but does not prevent formation of arabinogalactan
newly synthesised still have protective cell wall
will not die from osmotic instability/ autolysis
Outline the role of antibiotics in the treatment of infectious diseases, such as TB.
kill bacteria by causing bacteria to lyse
prevents bacterial growth/ prevents bacterial replication
antibiotics interferes with the modulation of chromosomal supercoiling through topoisomerase- catalyses
strand breakage and rejoining reactions is required for DNA synthesis, mRNA transcription and cell division
prevents protein synthesis (initiation and elongation)/ inhibit RNA polymerase
antibodies may also result in protein mistranslation by promoting tRNA mismatch with mRNA codon
Antibiotics may also inhibit cell membrane function which result in leakage of important solutes essential for
cell's survival
Do not affect human cells/ tissues/ not toxic to humans

From passgae, 'Isoniazid is administered as a prodrug, and must be activated by a bacterial enzyme known as KatG. Upon
activation, isoniazid inhibits the action of fatty acid synthase, inhibiting synthesis of mycolic acids and thus preventing the
synthesis of the mycobacterial cell wall..'
Explain how strain K131 is resistant to isoniazid. [4]
KatG is located in the 2.0-2.5Mb region
mutation to the gene would alter the mRNA encoded
amino acid sequence of KatG is altered
affect folding of KatG
change in conformation of active site -- rmb: activation <--> active site also keyword: bind
unable to bind to isoniazid to activate it talking about how resistance conferred prevents activation of drug
fatty acid synthase function not inhibited --talking about how resistance conferred inhibits function of the drug
mycolic acids still synthesised

Using a named disease, discuss how vaccination is an effective measure to control the disease. [11]
caused by Variola minor virus
infect respiratory tract, lymphatic system, skin
prolonged direct face-to-face contact, direct contact with infected bodiliy fluids or contaminated objects
mass vaccination programme to achieve vaccination in 80% of the populations in each country
Infectious disease:
disease caused by a pathogen
transmissible/ passed from one organism to another
Affects the normal functions of the body

Suggest why TB is more likely to be fatal in people who have HIV/AIDS than in those who do not have HIV/AIDS.
HIV/ AIDS leads to weak immune system
details: reduced action of phagocytes, T helper cells low in number, B cell response is low
(so TB) pathogens can multiply faster are not destroyed before they cause disease
Idea that important organs may already be suffering from consequences of HIV/ AIDS (so more likely to stop functioning)
ref to inactive/dormant/latent TB more likely to become active