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Michaelmas Flashcards

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1
Q

What is the difference between aetiology and pathogenesis?

A

Aetiology - causes of disease
Pathogenesis - how diseases develop

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2
Q

What are the various factors causing disease?

A

Lack of ATP, O2
Trauma
Excessive immune response

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3
Q

What is oxidative stress?

A

Production of ROS and NO, damaging cells

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4
Q

What are the consequences of reperfusion injury?

A

Damage to cells when oxygenated blood returns
Can lead to inflammation and recruitment of leukocytes

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5
Q

What are the downstream affects of impaired energy homeostasis?

A

Na/K activity decreases, causing build up
Glycolysis resulting in a build up of lactic acid
Ribosome detachment

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6
Q

What factors affect cellular response to injury?

A

Type, duration and severity of injury

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7
Q

What are the cellular responses to stress?

A

Atrophy- reduce size
Hypertrophy - increase size
Hyperplasia- increase number
Metaplasia - replace cell type with another

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8
Q

What are examples of positive and negative stresses on cells?

A

Positive- preganancy, high intensity workouts
Negative - swelling, injury, exposure to toxic chemicals

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9
Q

What are the key protein-related mechanisms cells use to respond to stress? (4)

A
  1. Heat shock proteins - activation of heat shock factors (HSF), and HSP for stress resistance
  2. Unfolded protein response - synthesis of chaperones to ensure correct folding
  3. Ubiquitin degradation of unfolded proteins
  4. Stress-kinase pathway - Activation of JNK/SAPK and p38 kinase pathway
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10
Q

What are the distinguishing characteristics between necrosis and apoptosis?

A

Necrosis - uncontrolled, leads to inflammation
Apoptosis - controlled, occurs intrinsically, or can be extrinsically activated

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11
Q

What is the definition of commensals in the context of organisms, and what distinguishes them from harmful pathogens?

A

Commensals refer to organisms that benefit from another without causing harm. Unlike harmful pathogens, commensals coexist without causing disease.

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12
Q

What characterizes sterile inflammation, and under what conditions does it occur?

A

Sterile inflammation is inflammation that occurs with no microbial target. Triggered by non-infectious factors, such as tissue damage or autoimmune responses.

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13
Q

When do opportunistic pathogens typically cause disease?

A

Rarely causes disease unless host defence is compromised

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14
Q

How much of the human genome is involved in defense?

A

10% of human genes

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15
Q

What is the energy usage difference between the resting and activated immune systems?

A

1600kJ resting, and activated 6000kJ

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16
Q

Describe the different immune responses for extracellular and intracellular pathogens.

A

For extracellular pathogens, phagocytes and antibodies
For intracellular pathogens, often leads to cell death

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17
Q

What are some examples of physical and chemical barriers?

A

Skin
Mucus
Keratin

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18
Q

How does innate immunity differ from adaptive immunity?

A

Innate immunity is immediate and poised for action, involving components like macrophages
Adaptive immunity takes time to develop but has a faster secondary response, and involves B and T cells

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19
Q

What are the steps in the acute inflammatory response?

A
  1. Breaching of barriers
  2. Release of PAMPs
  3. Detection by cells containing PRR
  4. Release of histamines
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20
Q

What are the physical and secretory components of epithelial barriers?

A

Physical include - squamous epithelia, cilia, and keratin
Secretory - mucus, stomach acid, and antimicrobial enzymes

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21
Q

What are the key cell types in the myeloid and lymphoid lineages?

A

Myeloid lineage includes - macrophages, dendritic cells, mast cells, neutrophils, basophils, and eosinophils
Lymphoid lineage includes - NK cells, B and T cells

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22
Q

What are the features of cytokines?

A

Redundancy
Pleiotropism - many effects
Antagonism - block each other
Synergy - work together

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23
Q

What are the three main groups of cytokines?

A

Interferons
Interleukins
Tumour necrosis factors (TNF)

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24
Q

What are the characteristics of Pathogen-Associated Molecular Patterns (PAMPs)?

A

High conserved, essential for pathogen survival
Examples: DNA, flagellin, coat proteins

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25
Q

What is the role of Pattern Recognition Receptors (PRR), and where are they located?

A

Germ line receptors located either intracellularly (endosome) or on the cell membrane
Stimulate phagocytosis and immune responses

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26
Q

Describe the Toll-like receptor family, including the types of TLRs and their locations

A

Types of PRR, dimerises, phosphorylates TF, activates production of cytokines
e.g. TLR4 detects Lipopolysaccharides (LPS) from gram-negative bacteria
TLR 3,7,8,9 are located on endosomes, mainly for viruses that have inserted their genome

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27
Q

What are some examples of other PRRs?

A

C-type lectin receptors (CLR) for fungal infections
Cytosolic NOD-like receptors (NLRs) that detect PAMPs and DAMPs in the cytoplasm

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28
Q

What is the role of the inflammasome?

A

NOD-like receptors assemble a protease containing Casp-1 instead of a signaling cascade for transcription factor activation
Casp1 cleaves interleukins, activating inflammation

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29
Q

What are Damage-Associated Molecular Patterns (DAMPs)?

A

Molecules released from damaged tissue
e.g. DNA, heat shock proteins, damage mitochondria

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30
Q

What are mast cells, and what role do they play in the inflammatory response?

A

Prebound to IgE, trigger inflammation rapidly by the release of histamine during degranulation.
Also secrete prostaglandins

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31
Q

What functions do macrophages perform in the immune response?

A

Phagocytose microbes and produce cytokines
e.g. IL-1β, TNF-α, and IL-6

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32
Q

What is the role of dendritic cells in the immune response?

A

Memory cells that take antigens to the lymph node to activate T cells, which, in turn, activate B cells.

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33
Q

What are the steps involved in the recruitment of leukocytes from blood vessels?

A

Rolling, tight adhesion, diapedesis (extravasation), and migration (down CXCL8 gradient)
Selectins, integrins, and IgSF facilitate this movement.

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34
Q

What are the beneficial and pathogenic effects of TNF-α?

A

TNF-α has beneficial effects such as stopping pathogen entry but can lead to hyper-response, causing sepsis.
TNF-α triggers blood clotting, leading to organ failure

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35
Q

What are the passive and active methods for switching off inflammation?

A

Passive - utilizing the short half-lives of mediators and neutrophils
Active- macrophages switching from pro to anti-inflammatory states, the release of anti-inflammatory cytokines, and lipid mediator class-switch.

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36
Q

What processes are involved in repair and healing?

A

Macrophages phagocytosing debris
Producing ROS and NO
Recruiting fibroblasts, and angiogenesis
Fibroblasts increase collagen synthesis

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37
Q

What is the process of activation in the Antigen-Antibody (Classical) reaction, and what are the outcomes?

A

C1 recognises antigen-antibody interaction, this leads to the activation of a C3 convertase which increases chances of the C3 threshold being reached

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38
Q

Describe the alternative complement pathway

A

Spontaneous hydrolysis of C3 to C3a and C3b occurs, addition to a component of Factor B forms C3bBb

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39
Q

Describe the lectin-mannose complement pathway

A

Triggered by mannose on Nisseria, forms the Mannose Binding Lectin Associated Serine Protease (MASP). This triggers the conversion of C3 to C3a and C3b

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40
Q

What are the effects of the complement pathway?

A

Opsonisation - C3b flags, to aid phagocytosis
Cell lysis (MAC, C5b6789)
Chemotaxis - via C5a
Activation of mast cells (C3a, C4a, C5a)

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41
Q

What are the regulatory controls for the complement pathway?

A

Short half-life
Properdin factor P (promotes)
Factor I degrades
Membrane cofactor protein (MCP) and DAF dissociates C3bBb so Factor I can bind
Factor H binds to sialic acid, flags as mammalian cell, dissociates C3bBb
Protectin stops MAC formation

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42
Q

What are examples of complement deficiencies and what do they lead to?

A

C1-C4 = Immune complex, unable to clear
C5-C9 =Susceptibility to Neisseria
Factor I and H = C3 depletion
DAF, Protectin = Auto-immune diseases

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43
Q

What is adaptive immunity, and what are its components?

A

Adaptive immunity recognises pathogens with specificity, and can create a memory response. Components are B and T cells

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44
Q

What is clonal expansion, and when does it occur?

A

Proliferation and differentiation of lymphocytes
Occurs when lymphocytes are activated by binding specifically to a complementary antigen.

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45
Q

What are B lymphocytes, and what is their role in the immune system?

A

B cells are generated in the bone marrow, and activated in germinal centres in secondary lymph nodes.
Then can differentiate in plasma cells and secrete antibodies

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46
Q

What are their variable and constant regions on antibodies responsible for?

A

Variable regions interact with antigens
Constant regions recruit effector functions.

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47
Q

What are the three main antibody effects?

A

Neutralization blocks biological activity
Opsonization coats pathogens to enhance phagocytosis
Complement activation recruits complement for immune responses.

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48
Q

What are T lymphocytes, where are they generated and mature?

A

Produced in the bone marrow and maturate in the thymus

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49
Q

What is the function of Major Histocompatibility Complex (MHC) Class I?

A

Present internal antigens to CD8 Cytotoxic T cell

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50
Q

What is the function of MHC Class II?

A

Present external antigens to CD4 T cells

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51
Q

What are the three signals required for T cell activation?

A

TCR recognition of MHC
B7/CD28 interaction
Cytokine stimulation

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52
Q

What is the route dendrites take from the site of damage, to activating the immune system?

A

Dendrites travel via afferent vessel to the lymph node to the T cell area
T cells are activated and TfH interact with B cells in the germinal centre
This activates the B cells, and the dendritic cells leave via a vein

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53
Q

Describe the structure of antibodies

A

Variable light chain, specific to antigen (shows bispecificity)
Variable heavy chain, determines effector function (IgE, IgA, IgG, IgM, IgD)

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54
Q

What forms the antigen-binding site of antibodies, and what are the domains involved?

A

Antigen-binding site: interaction between heavy and light chain domains.
Domains are known as Complementary Determining Regions (CDRs), with CDR1-3, and CDR3 being the most variable.

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55
Q

How is antibody diversity generated?

A
  1. Somatic gene arrangement/recombination (VDJ).
  2. ALLELIC Exclusion- Different heavy and light chain combinations (2 types of light chains k and λ).
  3. Variable addition and losses of nucleotides.
  4. Somatic hypermutation by Activation Induced Deaminase (AID) in germinal centers.
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56
Q

Describe the process of somatic recombination in the generation of heavy chain diversity.

A

Rearrangement of multiple gene segments during B cell development, leading to sequence variation.
VDJ segments account for the variation in CDR3, allowing for 2 million variations.

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57
Q

Explain the process of affinity maturation in the germinal centers

A
  1. B cells endocytose the antigen and BCR.
    2.Antigen is broken down.
  2. Peptides are presented on MHCII to T follicular helper (TfH) cells.
  3. TfH recognizes and presents CD40L to CD40 receptor on B cell.
  4. Activated B cell moves into the dark zone of the germinal center.
  5. In the dark zone, B cells undergo proliferation.
  6. B cells move out into the light zone, competing for the antigen.
  7. Follicular Dendritic Cells (FDC) display the antigens.
  8. High affinity B cells undergo clonal expansion, maturation
  9. Differentiated cells include plasma cells, long-lived plasma cells, and memory B cells.
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58
Q

What is the purpose of corroboration of non-self in the immune response?

A

Corroboration involves Dendritic cells, T (CD4) helper cells, and B cells presenting to each other to confirm that the antigen is non-self. Tackle autoimmunity

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59
Q

What is isotype switching, and what does it involve?

A

Switching constant regions
Original immunoglobulin formed is either IgM or IgD, followed by a change in constant regions to IgG, IgA, or IgE isotypes

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60
Q

How is alternative splicing involved in antibody generation?

A

Generates both B cell receptors (BCR) and soluble antibodies
Addition of a polyA tail to the mRNA transcript determines whether the antibody will be released as a soluble form

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61
Q

Define affinity and avidity in the context of antibodies.

A

Affinity- interaction between the antibody binding site and the epitope of the antigen.
Avidity- strength of interaction due to polyvalent epitopes, representing the sum of individual affinities

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62
Q

Name the specific activities associated with each antibody isotype.

A

IgE = Priming mast cell for degranulation
IgA = delivery of antibodies to mucosal surfaces
IgG= Opsonization, ADCC, activation of eosinophils
IgM = Opsonization, activation of complement
IgD = corroboration of non-self

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63
Q

What are the similarities and differences between Class I and Class II MHC?

A

Similarities:
- Both are cell surface glycoproteins.
- Both present peptides.
- Both are trans-membrane.
Differences:
-Class II has 2 trans-membrane components, while Class I has 1.
-Class II has α1 and β1 distal and α2 and β proximal, whereas Class I has a β2-microglobulin and α3 proximal, then α1 and α2 distal.

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64
Q

What is the role of the peptide binding groove in MHC molecules?

A

The groove is the location where peptides bind with high specificity
Class I:
-Has 6 groove pockets labeled A-F.
-Presents 8-9 amino acid length peptides.
Class II:
- Has an open-ended groove.
-Presents 13-25 amino acid length peptides.

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65
Q

Explain MHC diversity and the mechanisms that contribute to it

A
  1. Polygeny
    - Multiple genes HLA- A, HLA- B, HLA- C
  2. Polymorphism
    - Presence of multiple alleles
  3. Co-dominantly expressed (both maternal and paternal)
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66
Q

What are the mechanisms of antigen processing for MHC Class I?

A
  1. Proteins broken down by proteasome in the cytosol.
  2. Transporter Associated Processing (TAP) translocates peptides to the ER.
  3. Peptides loaded onto Class I molecules assisted by chaperone proteins.
  4. Forms Peptide Loading Complexes (PLC) and follows a secretory pathway to the cell surface.
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67
Q

What are the mechanisms of antigen processing for MHC Class II?

A
  1. Extracellular antigens taken up into the cell by endosomes.
  2. Acidification leads to activation of proteases in endosomes.
  3. Endosomes fuse with vesicles containing MHC Class II.
  4. Peptides loaded onto MHC II and presented at the cell surface.
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68
Q

Name the genes involved in antigen presentation (on MHC)

A
  1. Regulating peptide loading in MHC II = HLA-DM and HLA-DO.
  2. Transporter Associated with Antigen Processing (TAP) = TAP1 and TAP2.
  3. Loads peptide onto MHC I = TAP binding protein (TAPBP).
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69
Q

What are the key differences between the structure of T cell receptors (TCRs) and antibody Fab structures?

A

TCR Structure:
Monovalent with one binding site.
Membrane-bound.
Doesn’t undergo somatic hypermutation like BCRs.
Solely for antigen recognition.
Fab Structure (Antibody):
Bivalent with two binding sites.
Not membrane-bound.
Undergoes somatic hypermutation.
Functions in various roles, not solely antigen recognition.

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70
Q

What are the steps involved in T cell diversity generation?

A
  1. Rearrangement of β chain (VDJ segments).
  2. Cell proliferation.
  3. CD4 and CD8 expression.
  4. α chain rearrangement (VJ).
  5. CD4+ CD8+ double positive cell expression.
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71
Q

Highlight the similarities and differences between T cell receptors (TCRs) and B cell receptors (BCRs).

A

Similarities:
RAG proteins used.
VDJ and VJ segments rearranged.
Splicing occurs later.
Differences:
TCRs exhibit greater junctional diversity, eliminating the need for somatic hypermutation.
Total Diversity: TCRs have 10^18, while Immunoglobulins have 5x10^13.
No post-development mutation occurs for TCRs.

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72
Q

What is the process of positive selection in T cell receptor development?

A
  • T cells are tested against self-peptide complexes on cortical epithelial cells in the (Cortex of thymus)
  • “Moderate affinity” interactions lead to a positive signal for maturation.
  • Lack of signal results in apoptosis (death by neglect).
  • CD4 and CD8 selection depends on whether presented against MHC I or MHC II.
  • Negative selection occurs in the medulla
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73
Q

Explain the significance of negative selection in T cell receptor development.

A
  • Avoids the development of autoimmunity.
  • High affinity for self-peptides may indicate previous exposure or a component of the body
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74
Q

How is T cell receptor signalling initiated?

A

Binding causes
1. CD4 and CD8 to activate tyrosine kinase (LCK).
2. LCK phosphorylates immunoreceptor tyrosine-based activation motifs (ITAMS).
4. Phosphorylation cascade
5. PLCγ and RAS activation
6. Production of cytokines such as IL-2 occurs.
7. PLCγ produces IP3, releasing Ca2+ from the ER.

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75
Q

What are the effector functions of CD8 T cells upon activation?

A
  1. Produce Perforin and Granzyme B to signal apoptosis.
  2. Proliferate in the presence of IL-2.
76
Q

Describe the primary antigen response and the steps involved in B cell activation.

A
  1. BCR binds to antigen
  2. Receptor is endocytosed
  3. Broken down an presented on MHC II
  4. Activates CD4 T helper cells
  5. Corroboration leads to secretion of IL4 and IL2 and B cell activation
  6. Costimulation of CD40 also required
  7. B cells undergo clonal expansion and differentiation into memory cells
77
Q

What are innate lymphocytes, and how do they resemble T cells?

A

Resemble T cells but lack TCR.
Subset mirrors T helper cell lineage, activated by the same cytokines.
-> Faster response than T cells.

78
Q

Explain the concept of cross inhibition among T helper cells.

A

Inhibitory signals that occur between different subsets of T helper (Th) cells. Examples:
1. Treg - produces TGF-β, inhibits TH1 and TH2
2. TH1 - produces IFN-γ, inhibits TH2 and TH17
3. TH2- produces IL-4, inhibits TH1 and TH17

79
Q

What is the Th1 and Th2 response?

A

Th1 cells are associated with responses against intracellular pathogens
Th2 cells are involved in responses against extracellular parasites and allergic reactions.

80
Q

Define tolerance and differentiate between central and peripheral tolerance.

A

Tolerance - State of unresponsiveness to substances or tissues.
Central tolerance- occurs during lymphocyte development, includes positive and negative selection
Peripheral tolerance - occurs after lymphocytes leave the primary organs

81
Q

What are the factors affecting tolerance?

A

Timing.
Dose of antigen.
Amount of co-stimulation.
Location

82
Q

Explain the limitations of central tolerance and how AIRE overcomes some of these limitations

A

Limitations- Many antigens not expressed in the thymus or bone marrow
AIRE- Transcription factor turning on transcription of ‘peripheral’ genes in the thymus
APS-1 autoimmune condition if lacking AIRE

83
Q

Describe the BCR selection process

A
  1. B cells reacting to self-cells are eliminated during development.
  2. Self-reactive cells can undergo receptor editing.
  3. Receptor editing involves replacing the light chain on the receptor.
  4. High doses of soluble proteins result in anergy.
84
Q

List and briefly explain the five mechanisms of T cell tolerance

A
  1. Ignorance- presence of privileged sites
  2. Split tolerance - T cell without B cell tolerance, T cells so can only produce IgM
    receptors and not IgG
  3. Anergy - only one signal, no B7/CD28
  4. Treg suppression- secrete anti-inflammatory cytokines
  5. T cell exhaustion- present PD1, and T signalling suppressed
85
Q

What are the properties and roles of Regulatory T cells (Tregs)?

A

Expression of IL-2 CD25 receptors and transcription factor FOXP3.
Roles:
1. Suppress proliferation of naive T cells.
2. Secrete anti-inflammatory cytokines (e.g., IL-10, TGF-β).
3. Cytolysis: Release of Granzyme, forming a perforin pore.
4. Metabolic disruption: Adenosine acting as immunosuppressive.
5. Target dendritic cells via CTLA4-CD80/CD86 interaction.

86
Q

What are the properties of exhausted T cells?

A
  1. Present PD1 (similar to CD28).
  2. Bind to ligands PD-L1 and PD-L2.
  3. Suppress T cell signaling, rendering the cell less responsive.
87
Q

What is the role of adjuvants in tolerance? Provide an example.

A

Used for - allergen-specific immunotherapy. dampen effects of allergy
- modulate immune responses by promoting regulatory T cell (Treg) responses
- activation of immune cells involved in tolerance induction
Complete Freund’s Adjuvant: Contains ground-up mycobacteria.

88
Q

Define autoimmunity and briefly explain its common cause

A

Response to self-antigens, often due to the failure of self-tolerance

89
Q

Describe the hygiene and the cryptic hypothesis

A

Hygiene Hypothesis: Reduced exposure to infectious diseases early in life increases susceptibility to autoimmune diseases
Cryptic Hypothesis: Suggests that chronic viral infections are related to the development of autoimmune diseases.

90
Q

List and briefly explain the three mechanisms of autoimmune pathology.

A
  1. Direct Antibody-Mediated Effects: Autoantibodies cause immune cells to attack specific organs.
  2. Immune Complex-Mediated Effects: Binding of complement components and transport to liver/spleen, e.g., Lupus/SLE.
  3. T Cell-Mediated Effects: T cell-mediated damage and tissue destruction, e.g., Multiple Sclerosis, Type 1 Diabetes, Rheumatoid Arthritis.
91
Q

Explain the antibody-mediated effects in Graves’ disease and Hashimoto’s thyroiditis.

A

Graves’ Disease: Antibody binds to TSH, leading to constant activation and production of thyroid hormones.
Hashimoto’s Thyroiditis: CD4 and CD8 T cells destroy the gland, mostly involving a Th1 response.

92
Q

What are the effects of Lupus/SLE?

A
  1. Failure to remove complement complexes can block vasculature or deposit on endothelium
  2. Auto-antibody production by B cells
  3. T helper imbalance, less Treg, more pro-inflammatory
  4. Cytokine dysregulation - storm = more inflammation
93
Q

Discuss T cell-mediated diseases

A

Multiple Sclerosis: T cells damage the myelin sheath, impairing nerve transduction.
Type 1 Diabetes: T cells attack insulin-producing β-cells, causing high blood glucose levels and vascular/neurological damage.
Rheumatoid Arthritis: Autoreactive CD4 T cells and antibodies forming immune complexes contribute to joint destruction.

94
Q

What are the genetic and environmental factors associated with autoimmune diseases?

A

Genetic Factors:
- HLA allotypes, polymorphic variations affecting MHC class II receptors.
- Sex differences, with women more likely to develop autoimmune diseases.
Environmental Factors:
- Infections, as per the Cryptic Hypothesis.

95
Q

Explain the initiation of autoimmune diseases

A

Protein modification, e.g., citrullination, by environmental factors leading to self-tolerance breakdown.
Autoimmune sympathetic ophthalmia: Damage to one eye releases sequestered antigen, causing an attack on the contralateral eye

96
Q

Discuss the perpetuation of autoimmune diseases

A

Molecular Mimicry: Antigens of pathogens resemble host structures, leading to cross-reactivity.
Examples: Coeliac Disease: Involves enzyme modification and immune response activation.
Rheumatoid Arthritis: Protein modification linked to smoking.

97
Q

What are some treatments for autoimmune diseases, and how do they work?

A
  1. Organ-Specific Treatments:
    Thyroxine for hypothyroidism, insulin for Type 1 Diabetes.
  2. Immunosuppressive Drugs:
    Steroids, Cyclosporin (inhibits IL synthesis), Rapamycin (G1 arrest), Fingolimod (prevents lymphocyte migration).
  3. Antibodies to TNF-α or its Receptors: Acts as an anti-inflammatory response by blocking cytokine effects.
  4. CTLA4-Ig: Binds to CD80/CD86 with high affinity, preventing co-stimulation of T cells and initiation of an autoimmune response.
98
Q

Define hypersensitivity and briefly explain its nature

A

Immune responses that are damaging rather than helpful to the host, caused by over-reaction

99
Q

List and briefly describe the four types of hypersensitivity

A
  1. Type I Hypersensitivity:
    Mediator: IgE
    Examples: Allergies, asthma, hay fever.
  2. Type II Hypersensitivity:
    Mediator: IgG and IgM antibodies
    Examples: Blood transfusion reactions, destruction of red blood cells.
  3. Type III Hypersensitivity:
    Mediator: Immune complexes
    Examples: Serum sickness, Arthus reaction.
  4. Type IV Hypersensitivity:
    Mediator: T cells (Th1)
    Examples: Contact dermatitis, tubercular lesions.
100
Q

Explain the mechanism and examples of Type I hypersensitivity

A

IgE response mediated by Th2 cells.
- Sensitization and re-exposure lead to rapid response and degranulation of mast cells.
Examples: Systemic anaphylaxis, wheal and flare, hay fever, asthma, food allergies.

101
Q

Explain the effects of products associated with Type I hypersensitivity

A

Histamine - increased vascular permeability, anticoagulation.
Cytokines: IL4, IL13, IL33, IL3, IL5 - amplify Th2 cell response, promote eosinophil production.
Chemokine: CCL3 - attracts monocytes, macrophages.
Lipid Mediator: Prostaglandins - smooth muscle contraction, mucus secretion, attracts leukocytes.

102
Q

Explain Type II hypersensitivity with a focus on blood transfusion reactions

A

Blood Transfusion: Mediated by IgM or IgG antibodies.
ABO blood group variations, H antigen differences.
Rh factor - Rh-positive can cause issues in Rh-negative individuals.

103
Q

Discuss Type III hypersensitivity, including its association with vaccine reactions

A

Commonly associated with vaccine reactions (Arthus).
- Occurs when antigens are soluble and in high concentration.
Triggers mast cells via FcγRIII receptor, leading to tissue damage and inflammation.
Examples include Arthus reaction, serum sickness.

104
Q

Explain Type IV hypersensitivity

A

Mediated by T cells (Th1), releasing cytokines.
Examples include contact dermatitis, TB granulomas.
- Requires higher concentrations of antigens, and a Th1-stimulated response.

105
Q

Define iatrogenic and provide examples.

A

Causation if disease due to medical treatment, such as blood transfusion.

106
Q

Differentiate between natural, autologous, syngeneic, allogeneic, and xenogeneic transplants

A

Natural: Such as pregnancy.
Autologous: Own graft.
Syngeneic: From an identical twin.
Allogeneic: Same species but genetically distinct organisms (most common).
Xenogeneic: Between two different species.

107
Q

Explain the role of T memory cells in grafts

A

Initial graft leads to a long response and rejection.
Second graft from the same donor leads to a faster, greater response.
Third graft from a different donor has the same response as the first graft.

108
Q

What are the mechanisms of rejection?

A

Hyperacute
Acute
Chronic

109
Q

Discuss the mechanisms and examples of hyperacute rejection

A

Dependent on pre-existing antibodies.
Examples: Previous organ transplants, pregnancy (Rhesus antigens), blood transfusion (ABO blood groups), xenotransplants.

110
Q

Explain acute rejection in transplant situations

A

Direct Recognition: Recognizes that MHC receptors are foreign on the transplant.
Due to different combinations of HLA allotypes.
Indirect Recognition: Recognizes foreign proteins (e.g., H antigens).
Leads to immune complex formation and Antibody-Dependent Cell-mediated Cytotoxicity (ADCC).

111
Q

Describe chronic rejection in transplant situations

A

Occurs years after transplant.
- Gradual formation of immune complexes (Type III hypersensitivity).
Results in compromised blood supply, ischemia, and loss of function

112
Q

Discuss Graft versus Leukemia (GvL) and Graft versus Host Disease (GvHD)

A

GvL - donor T cells kill residual leukemia.
GvHD - T cells in donor tissue attack host cells.

113
Q

Explain how HLA matching is determined in transplantation

A

Luminex bead-based Cross-matching: Involves testing for pre-existing antibodies using luminex beads with HLA bound.
Genetic Screening: Screening for HLA compatibility.

114
Q

Discuss the various immunosuppression methods used in transplantation

A
  1. Steroids: Mimic corticosteroids, reduce inflammation.
  2. Azathioprine: Leads to death of rapidly dividing T cells.
  3. Cyclosporin: Inhibits Ca2+ signaling.
  4. Rapamycin: Causes G1 arrest of proliferating cells.
  5. CTLA4-Ig: Prevents CD28 co-stimulation.
  6. Treg Cells: Removed, expanded, and re-injected for tolerance.
  7. Autologous Stem Cells: Potential for regenerative purposes.
115
Q

Discuss hematopoietic transplants, adoptive T cell therapy, and chimeric antigen receptor (CAR) therapy.

A

Hematopoietic Transplants: Uses peripheral blood cells, bone marrow, umbilical cord blood.
- Corrects inborn errors of immunity, reconstitutes the immune system.
Adoptive T Cell Therapy: Involves isolation, purification, expansion, and infusion of tumor-reactive T cells.
Chimeric Antigen Receptor (CAR): Different receptor on the cell, recognizes foreign antigens.
- Approved to treat B cell leukemia by removing all B cells.

116
Q

How was the presence of a virus discovered?

A

Passing a homogenised fluid through a filter, that removed bacteria and fungi and then reinfecting cells. e.g. TMV

117
Q

List five characteristics of viruses.

A
  1. Small size, typically 20-200nm (largest is 2300nm)
  2. Obligate intracellular parasites
  3. Replicate uniquely, depending on type of genome (RNA, DNA)
  4. Sometimes contain an envelope
  5. Lack intracellular structures/ organelles
118
Q

Why do RNA genomes evolve rapidly?

A

Due to the error- prone nature of the RNA-dependent RNA polymerases, which lack proof-reading mechanisms

119
Q

Name techniques used to measure viruses and what information each technique provides

A

Electron microscope - to see the structure of the virus
Polymerase Chain Reaction - used to identify and quantify virus genomes
Haemagglutination- viruses (Flu) bind to RBC receptors
Plaque assay - to measure infectivity
Quantification of immune response

120
Q

Outline the six steps involved in the replication of viruses.

A
  1. Finding cell
  2. Adsorption/ Attachment
  3. Penetration/ Endocytosis
  4. Eclipse phase (no pfu)
  5. Assembly at the membrane
  6. Release
121
Q

What is the difference between monopartite and segmented virus genomes, and how does it impact virus diversity?

A

Monopartite- single nucleic acid molecule.
Segmented - several nucleic acid molecules e.g. Influenza (8)
Allowing for recombination during assembly, if two versions of a virus infect the same cell e.g. avian and human flu

122
Q

Name features in viruses that increase their coding potential that contribute to their complexity.

A
  1. Overlapping reading frames - can code for more than 1 protein.
  2. Ambisense - codes proteins from both directions.
  3. RNA splicing
123
Q

Define the terms “latent period” and “mean burst size” in the context of viruses

A

Latent period- Time taken to form new virus particles
Mean burst size- Average yield of viruses from a cell, using plaque assay

124
Q

Where do most DNA viruses replicate, and what is the exception to this rule?

A

Mostly replicate in the nucleus, except poxvirus, which replicates in the cytoplasm

125
Q

Where do most RNA viruses replicate, and what is the exception to this rule?

A

Most RNA viruses replicate in cytoplasm, except influenza which replicates in the nucleus as it carries out cap-snatching and so requires host DNA-dependent RNA polymerase

126
Q

What are the key structural differences between positive viral RNA and host mRNA?

A

Positive viral RNA lacks a 5’ cap and Poly A tail, and it has a distinctly different structure from host mRNA.

127
Q

Outline the steps involved in the replication of retroviruses, including the key enzymes they use.

A
  1. Insertion
  2. Reverse transcription by RNA-dependent DNA polymerase
  3. Formation of dsDNA, integrated into host nucleus by integrase
  4. Formation of provirus, behaving like host DNA
  5. Uses host DNA-dependent RNA polymerase II to form mRNA, followed by packaging, splicing, and translation.
128
Q

Why is temporal control important in virus gene expression, and provide an example of viruses with temporally distinct gene classes.

A

Temporal control is crucial as different proteins are needed at different stages of the life cycle. - For example, Herpes and poxviruses have temporally distinct gene classes expressed in a regulated cascade.

129
Q

What is ribosomal frameshifting, and why is it significant in viruses?

A

Ribosomal frameshifting occurs when ribosomes slip into another open reading frame, resulting in a different amino acid sequence. This maximizes coding capacity, as seen in SARS-CoV-2.

130
Q

What are the two main methods of virus assembly, and how do they differ?

A
  1. Spontaneous self-assembly: Polymerization of protein subunits leading to encapsulation of capsid and genome.
  2. Complex multiple staged: Assembly of capsid, followed by insertion of the genome and envelope formation.
131
Q

How do retroviruses establish latent infection, and how is a latent infection with Herpes different?

A

Insertion of viral DNA into host DNA, to form provirus. Not always transcribed but causes a latent infection.
With Herpes, the viral DNA is not integrated into the host DNA, and remains as an episome

132
Q

What does subversion in virus-host interaction refer to?

A

Takeover of cellular processes.
For example DNA viruses using host machinery to transcribe genome

133
Q

What are examples of host modifications carried out by viruses?(6)

A
  1. Subversion
  2. Stimulation of biochemistry (dNTPs), by Pox and Herpes
  3. Cytopathic effect (cpe)
  4. Cell membrane modifications
  5. Cell transformation (cancer)
  6. Suppression of host immune signalling
134
Q

Provide examples of viruses and their corresponding portals of entry.

A

Oropharynx: Herpes, Epstein-Barr virus
Respiratory Tract: Influenza, Measles, Chickenpox
Conjunctiva: HSV
Skin: HPV, Rabies
Blood: Yellow fever virus, Hepatitis B, HIV

135
Q

What are examples of host physical barriers?

A
  1. Skin
  2. Cilia
  3. Mucous
  4. Proteases
  5. Microbiome
136
Q

How do viruses adapt to suppress complement?

A

Viruses can steal host proteins like CD46, CD55, and CD59 for their envelope, suppressing complement

137
Q

Name the three types of interferons and their functions.

A
  1. Type I (IFNα and IFNβ): Released by infected cells, up-regulates class I MHC.
  2. Type II (IFNγ): Released by T cells and macrophages, promotes Th1 immunity.
  3. Type III (IFNλ): Important in epithelial cells, with only some cells responding to them.
138
Q

In Type I IFN induction, what proteins are encoded to inhibit virus replication?

A
  • Signalling via JAK-STAT pathway
  • Protein Kinase R (PKR) and Mx protein are encoded, inducing the inhibition of host protein synthesis, preventing virus replication.
139
Q

Provide an example of a mechanism used by viruses to interfere with interferons.

A

Vaccinia virus, produce an IFN binding protein to disable the antiviral effects of interferons.

140
Q

How do viruses interfere with apoptosis?

A

Viruses can inhibit apoptosis by targeting and inhibiting proapoptotic proteins like Bax and Bad.

141
Q

How do viruses interfere with cytokines?

A

Viruses can secrete proteins that bind to cytokines. For example, Epstein-Barr virus secretes vIL-10, driving a Th2 response instead of Th1.

142
Q

What role does age and sex play in the outcomes of certain viral infections?

A

Varicella-zoster and SARS-CoV-2 are less dangerous in kids, and Hepatitis B is worse for males, increasing the risk of liver disease/cancer.

143
Q

How do viruses escape detection by the immune system?

A
  1. Block presentation of peptides on MHC
  2. Latency
  3. Mask Fc region on antibody
  4. Antigenic variation
144
Q

How do viruses interfere with chemokines?

A
  1. Sequestration (soak up)
  2. Chemokin mimicry (causing inappropriate signalling)
  3. Modulate signalling and host production pathways
145
Q

Provide examples of viruses that target the Central Nervous System (CNS).

A

Rabies- commonly fatal
HSV and VZV- rare but can prove fatal
Enteroviruses (Polio) - characterised by paralysis, rare

146
Q

What are the characteristics that differentiate superficial infections from systemic infections?

A

~Superficial infections replicate at the epithelium, don’t spread, have a short incubation period, and are acute (e.g., Influenza).
~Systemic infections replicate at the portal, spread to other organs, have a long incubation period, and can be severe (e.g., Smallpox, Measles).

147
Q

How does temperature affect the spread of viruses?

A

Effects the spread of viruses.
Rhino, thrive at 32°C but not at 37°C.

148
Q

Give examples of viruses and their modes of exit from the host.

A

Blood : HIV, Yellow fever, HCV, HBV
Respiratory: SARS-CoV2, Influenza
Placenta : Rubella, HCMV
Breast milk: HCMV

149
Q

Define the Reproduction (R) value in the context of viral infections.

A

The R value indicates whether an epidemic is expanding (R > 1) or declining (R < 1).
R0 represents infection spread without containment
Rt considers control measures.

150
Q

What are the different types of vertical transmission?

A
  1. Transplacental Infections: Rubella, HIV, Human CMV.
  2. Perinatal: During birth or from breast milk - Herpes Simplex Virus, Hepatitis B.
  3. Germ Line Transmission: Presence of retrovirus, e.g., Herpes Simplex Virus.
151
Q

Provide examples of viral infections and their impact.

A
  • SARS-CoV-2: Killed over 6.5 million.
  • Foot and Mouth Disease (FMDV): Epidemic in the UK in 2001 resulted in the culling of 6 million cows and sheep, with an £8 billion cost to the UK economy.
152
Q

What are the types of influenza, and how is their nomenclature determined?

A

Types: A (avian), B (humans), C, and D.
Nomenclature: Type/Location/Isolate number/Year.

153
Q

Describe the genome of influenza and the key steps in its replication cycle.

A

Genome: Segmented RNA (8 segments).
Replication Cycle:
1. Entry through HA binding to Sialic acid
2. Endocytosis and acidification via M2 channel.
3. Fusion of virus membrane to host membrane.
4. RNA genome release.
5. Transport to the nucleus for replication.

154
Q

Differentiate between antigenic drift and shift in influenza. Why is antigenic shift more concerning?

A

Antigenic Drift: Genetic mutations over time.
Antigenic Shift: Recombination of genetic segments (8 segments). More concerning due to sudden, major changes leading to pandemics.

155
Q

How is Hepatitis A transmitted, what are its manifestations, and how can it be prevented?

A

Transmission: Contaminated food and water.
Disease: Jaundice, acute infections.
Prevention: HAV vaccine.

156
Q

How is Hepatitis B transmitted, what are its manifestations, and how can it be prevented?

A

Transmission: Contaminated blood.
Disease: Acute (Jaundice) and Chronic (Liver disease, inflammation).
Prevention: Vaccination, screening of blood.

157
Q

How is Hepatitis C transmitted, what are its manifestations, and how can it be prevented?

A

Transmission: Contaminated blood.
Disease: Acute or chronic (common), leading to liver cirrhosis and cancer.
Prevention: Drugs, no vaccine

158
Q

What are prions, and what diseases do they induce? Provide examples.

A

Prions: Infectious proteins (not viruses).
Diseases: Transmissible Spongiform Encephalopathies (TSEs), chronic and neurodegenerative.
Examples: Scrapies in sheep, Kuru, variant CJD, BSE in cattle (mad cow disease).

159
Q

Describe the difference between normal and abnormal structures of the PrP (Prion) protein

A

Normal PrP: Alpha helical, GPI anchored, cell surface glycoprotein.
Abnormal PrP: Beta sheets, very stable, resistant to protease digestion.

160
Q

What are the treatment options and preventive measures for SARS-CoV-2?

A

Treatment: Dexamethasone (anti-inflammatory), Remdesivir (RdRp inhibitor), Paxlovid (polypeptide cleavage inhibitor), Mulnupiravir (mutation inducer).
Prevention: Social distancing, wearing masks, quarantine.

161
Q

How is HIV transmitted, and what are the characteristics of the HIV virion?

A

Transmission: Sexual partners, contaminated blood transfusions, mother-to-neonatal via blood.
Virion: Retrovirus, cone-shaped capsid, glycan shield.

162
Q

Describe the genome of HIV and the key steps in its replication

A

Genome: +ve ssRNA with long terminal repeats (LTR).
Replication: Binding of gp120 to CD4 on T helper cells, co-receptor binding (CCR5 or CXCR4), budding through membrane, leading to latent infections.

163
Q

Explain the pathogenesis of HIV and the treatment options

A

Pathogenesis: Infects CD4 T helper cells, transient drop in CD4 count, controlled by CD8 T cells.
Treatment: No vaccine, combinatorial therapy (e.g., AZT, protease inhibitors, Maraviroc).

164
Q

List some public health control measures against infectious diseases.

A
  1. Quarantine/ Slaughter (e.g. mad cow)
  2. Surveillance- reporting
  3. Good sanitary practices - hygiene
  4. Vector control (e.g. mosquitoes)
  5. Screening of blood (e.g. against HIV, Hep B and Hep C)
165
Q

What are the key targets for antiviral chemotherapy?

A

Nucleic acid, viral polymerases, proteases, neuraminidase, and HIV integrase.

166
Q

Provide examples of successful virus eradication events and explain why they were successful.

A
  1. Smallpox: Eradicated due to factors like no animal reservoir, vaccine effectiveness, and no antigenic variation.
  2. Rinderpest: Eradicated using a vaccine in 2011, virus infecting cattle and buffalo.
167
Q

What is the structure of fungi membrane and cell wall? (4)

A
  1. Mannoproteins
  2. Outer cell layer of β-glucans
  3. Inner layer of chitins
  4. Plasma membrane (ergosterols)
168
Q

What are the two main morphological forms of fungi?

A

Oval (bud) and Filamentous

169
Q

What are the two ways fungi can replicate, and what are the characteristics of asexual reproduction?

A

Reproduction: Asexual (Anamorph) and Sexual (Teleomorph).
Asexual Characteristics: Mitotic production of spores like conidium (external) and sporangium (internal); low water content, tough cell wall for dispersal.

170
Q

How do fungi obtain nutrition, and what are saprotrophs?

A

Nutrition: Fungi rely on preformed organic compounds; secrete enzymes for extracellular digestion.
Saprotrophs: Feed on dead plant or animal material, can damage property through hyphae mechanism, rarely parasitic.

171
Q

What are the structural and immune defenses against fungal infections?

A
  1. Structural Barrier: Damage or trauma can lead to fungal invasion.
  2. Commensal Bacterial Flora: Inhibits fungal replication.
  3. Host Immune System:
    - Detection of PAMPs by DCs, neutrophils, and macrophages
    - Th17 cells produce Il-17 and IL-22 that recruit neutrophils
    - ROS
    - Antimicrobial peptides
    - Complement pathway (MLB)
172
Q

List factors that increase susceptibility to fungal infections.

A
  1. Loss/Damage to Structural Barrier.
  2. Impaired Fungal Sensing (e.g., Dectin-1 deficiency).
  3. Impaired IL-17 Function.
  4. Impaired Function of Neutrophils.
  5. Impaired Number/Function of T Cells and Macrophages.
173
Q

What are the methods of diagnosing fungal infections, and how do anti-fungal drugs target fungi?

A

Diagnosis: In vitro culture, Detection of fungal polysaccharide/DNA, Tissue biopsy.
Anti-Fungal Drugs: Target specific parts like ergosterol, fungal microtubules, and cell wall (inhibit glucan synthesis).

174
Q

What is the main treatment for fungal infections?

A

Anti-fungal drug e.g. Amphotericin

175
Q

What are the characteristics of Histoplasma in its infection?

A

Becomes a budding yeast above 37 degrees
hsp60 - used for binding
α-1,3 glucan - for masking
Calcium binding protein (CBP) - survive macrophage vacuole

176
Q

What are the different modes of transmission for viruses?

A
  • Blood (transfusion), e.g. HIV, Zika, HepB and C
  • Vector e.g. Zika, Dengue
  • Air-borne e.g. Influenza, SARS-COV2
  • Faecal-oral e.g. HepA
  • Vertical (placental) e.g. HCMV, HIV
  • Direct contact
177
Q

What are the 4 paradigms of inflammation?

A

Calor - temp
Dolor - pain
Rubor - redness
Tumor - swelling

178
Q

What are the roles of bradykinins? (3)

A

From mast cells
- Promote vascular permeability
- Binds to noiciceptors sensing pain
- Promoter prostaglandin formation

179
Q

What are the 4 ways in which Treg cells suppress the immune system?

A
  1. Anti-inflammatory cytokines (IL-10 TGF-β)
  2. Cytolysis - Granzyme B
  3. Metabolic disruption
    - CD39 causes ATP-ADP
    - CD74 causes ADP- adenosine
    Adenosine is immunosuppressive
  4. CTLA4 binding to CD80(B7) on DCs, instead of CD28 on T cells binding to it
180
Q

Describe the development of lupus

A
  1. Immune complexes build up
  2. Trigger inflammation
  3. Over-activation of TLR
  4. Produce BAFF
  5. Increases antibody secretion
181
Q

Describe the development of Rheumatoid Arthritis (RA).

A
  • Caused by autoreactive T cells
    1. Secrete cytokines activates Matrix metalloproteinases (MMP) and RANK
    2. RANK activates osteoclasts
182
Q

Describe the development of coeliac disease

A
  1. Gluten broken down and presented on APCs
  2. Activate CD4 T cells, to activate B cells
  3. Release pro-inflammatory cytokines e.g. TNF-α
  4. Plasma cells produce autoantibodies such as anti-tTG and anti- EMA
  5. Cause inflammation and damage to intestines, lack of vili and epithelial lining
183
Q

Provide examples of antiviral drugs

A

Tamiflu (neuraminidase (NA) inhibitor, no cleavage of sialic acid, blocks exit Influenza)
Acyclovir (Pi added, analogue of dGTP, incorporated for Herpes SV)
Maraviroc (CCR5 inhibitor for HIV)
Abacavir (targets reverse transcriptase of HIV)

184
Q

How does HSV enter cells?

A
  1. glycoproteins (gB and gD) on virus binds to Heparan Sulfate proteoglycan (HSPG) on the surface of cells
  2. Tethering
  3. Fusion of membranes then occur to release genome
185
Q

How is BCR diversity generated?

A
  1. Somatic recombination (VDJ)
  2. Light chain recombination (k and lamda), with VJ
  3. Addition and loss of nucleotides
  4. Somatic hypermutation (post development)
186
Q

Give an example of complement activation against a virus

A

SARS-CoV 2
- one of the first responses
- however unrestricted activation promoted by the virus leads to endothelial dysfunction, thrombus formation and organ failure
- Noris et al., 2021

Biology of Disease (4 decks)

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