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Biology > Forensics, Disease And Immunity > Flashcards

Forensics, Disease And Immunity Flashcards

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1
Q

What are fingerprints?

A
  • impressions left by the friction ridges of a human finger
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2
Q

How are fingerprints developed?

A
  • formed between weeks 6-10 of foetal life
  • raised portions of the epidermis
  • movements of baby in the womb, speed of growth etc. affect the fingerprint pattern
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3
Q

What are the types of fingerprints?

A
  • arch
  • tented arch
  • whorl
  • loop
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4
Q

How are fingerprints left?

A
  • sweat and oil from sebaceous glands cover our fingers
  • leaves and impression of the friction ridges when we touch something
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5
Q

Name three ways to make fingerprints visible:

A
  • carbon aluminium or magnetic iron powder (sticks to grease)
  • ninhydrin (become purple with AA in sweat)
  • superglue vapour
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6
Q

How much of DNA codes for protein?

A

1%

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7
Q

What is non-coding DNA transcribed into?

A
  • functional non-coding RNA
  • transfer RNA, ribosomal RNA, regulatory RNAs
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8
Q

What are the other functions of non-coding DNA?

A
  • transcription functions
  • promoters, translation regulation of genes, introns, origins of DNA replication, centromeres and telomeres
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9
Q

What are STRs?

A

Non-coding DNA contains many short repeated sequences

  • 3-7 bases long and repeated from a few to many times
  • make up 3% of human genome
  • likely involved in chromatin folding and transcription regulation
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10
Q

Describe small tandem repeats?

A
  • STRs occur at the same locus on both homologous chromosomes
  • number of STRs at a particular locus can vary on each homologous chromosome
  • STRs are inherited like genes
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11
Q

How do STRs help identify people?

A
  • each individual has a large number of STR loci
  • this creates a unique DNA profile for each individual depending on the number of STRs at various loci
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12
Q

What is DNA profiling?

A

DNA fingerprinting

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13
Q

What is DNA profiling used for

A
  • forensic technique used in criminal investigations
  • parental testing
  • genealogical
  • medical research
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14
Q

How is the length of STRs determined?

A
  • using gel electrophoresis
  • separates DNA fragments according to size
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15
Q

What is gel electrophoresis

A
  • a method of separating DNA fragments according to size in an agarose gel by applying an electric field
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16
Q

What is step 1 of gel electrophoresis

A
  • mix agarose and buffer
  • microwave to melt agarose
  • cool, pour into mould
  • remove comb when gel set
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17
Q

What is step two in G.E

A

Loading the gel
- the gel is put into a tank with buffer
- DNA samples are loaded into the wells of the gel with a pipettes

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18
Q

What is step three of G.E?

A
  • electrodes are attached to gel tank
    (Cathode near wells, anode on opposite side)
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19
Q

Why do DNA fragments migrate from - to +

A

Because DNA is negatively charged

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20
Q

Why do small fragments migrate further in gel electrophoresis?

A
  • larger fragmented get caught in the matrix
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21
Q

What are two ways of visualising DNA banding patterns?

A
  • Staining the DNA directly
  • Southern blotting
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22
Q

How is DNA stained?

A
  • using ethidium bromide and then visualised under a UV lamp
  • ethidium bromide inserts itself between the base pairs in the double helix
  • it grows in UV light making DNA visible
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23
Q

What is southern blotting used for?

A
  • to visualise specific DNA fragments
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24
Q

Describe the southern blotting method

A
  • DNA is transferred to nylon or nitrocellulose
  • membrane buffer is drawn up through gel
  • membrane with bound DNA is removed
  • hybridisation
  • labelled DNA probe is visualised
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25
Q

Describe hybridisation:

A
  • membrane is incubated with radioactive or fluorescent DNA proble
  • (binds with target DNA via complementary base pairing)
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26
Q

What are the four factors to identify time of death

A
  • body temp
  • degree of muscle contraction
  • decomposition
  • entomology and succession
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27
Q

How is body temperature maintained?

A
  • heat released in metabolic reactions (e.g respiration)
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28
Q

How is core body temperature of a dead body measured

A
  • long thermoprobe via rectum or abdominal stab
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29
Q

Describe this graph

A

A:
- sigmoid curve
- plateau 30-60 mins
- metabolic reactions not fully stopped yet

B:
- linear decline of temperature can be used to estimate time of death (~1.5C/h)

C:
- body temperature reaches ambient temperature

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30
Q

Why does the body cool down when a person dies?

A

Respiration stops
- no more heat released by cells

Heat lost from body by radiation and evaporation

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31
Q

What affects initial core body temperature?

A
  • fever
  • hypothermia
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32
Q

What affects postmortem cooling?

A
  • environmental temperature
  • air movement (wind)
  • humidity/body found in water
  • SA/vol ratio
  • fat composition
  • body location
  • clothing
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33
Q

How does environmental temperature affect cooling?

A
  • the greater the temperature gradient and air movement the more quickly the body loses heat
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34
Q

How does humidity affect cooling?

A
  • the higher the humidity the more slowly the body loses heat by evaporation
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35
Q

How does a body being in water affect body temperature?

A
  • a body in water will lose heat more quickly due to the temperature gradient
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36
Q

How does a body being in water affect body temperature?

A
  • a body in water will lose heat more quickly due to the temperature gradient
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37
Q

Will a small or large body lose heat more quickly?

A
  • small due to a higher SA/Vol ratio
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38
Q

A high fat composition and clothes will…

A

Insulate the body

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39
Q

What is rigor mortis?

A
  • ‘stiffness of death’
  • after death muscles first relax, then stiffen and then relax again
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40
Q

Label the structure of a sarcomere

A

1 - myosin head
2- thick filament (myosin)
3 - thin filament (actin)

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41
Q

What cause the contraction of a sarcomere?

A
  • ATP, Ca2+
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42
Q

Describe the mechanism of muscle contraction:

A
  • myosin-ADP binds to actin
  • ADP is released resulting powerstroke: muscle contracts
  • ATP binds
  • myosin ATP is released from actin and muscle relaxes
  • ATP hydrolyses to ADP + Pi
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43
Q

Give a summary of rigor mortis development?

A
  1. Death: muscle cells become starved of oxygen
    - aerobic respiration
  2. Respiration becomes anaerobic
    - produces lactic acid
  3. pH falls inhibiting enzymes
    - anaerobic respiration stops
  4. ATP is no longer produced
    - myosin and actin permanently fixed in contracted state
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44
Q

Why does rigor mortis stop after ~36 hours

A
  • lysosomes break down and release enzyme to break down cell

Apoptosis

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45
Q

Why does rigor mortis start sooner when a person has drowned

A
  • uses a lot of ATP
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46
Q

What affects time of onset of rigor mortis

A
  • fitness -> atp storage
  • metabolism
  • ambient temperature
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47
Q

Why does rigor mortis start sooner when a person has drowned

A
  • uses lots of ATP
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48
Q

Why is rigor mortis of limited use in determing time of death

A
  • after 36 hours its gone
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49
Q

What is decomposition?

A
  • digestion of cells resulting in breakdown of tissues and release of carbon and nutrients (e.g nitrate and phosphate)
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50
Q

What are the five stages of decomposition?

A
  1. Fresh, initial decay
  2. Bloating, putrefaction
  3. Active decay
  4. Advanced decay
  5. Dry remains
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51
Q

Describe the fresh stage

A
  • 0-3 days after
  • autolysis
  • anaerobic bacteria in gut start to digest tissues and release gases (start of putrefaction)
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52
Q

Describe bloating/putrefaction

A
  • 3-10 days
  • increasing gas production by bacterial activity causes swelling of body and putrid odor
  • breakdown of haemoglobin leads to venous marbling of skin + green discoloration of abdomen
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53
Q

Describe active decay

A

(Black putrefaction)

10-20
- discolouration of skin changes to purple then black
- tissues start to soften and then liquefy
- flesh looks creamy
- loss of fluid and deflation of body

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54
Q

Describe advanced decay

A
  • 20-50 day
  • majority of internal tissue lost
  • body starts to dry out
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55
Q

Describe dry remains

A
  • 50 to 365days
  • soft tissue lost, leaving skin, bone and cartilage
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56
Q

What is autolysis

A

Self digestion of cells

  • when respiration stops, lysosomes release digestive enzymes which digest cell components
  • digestive enzymes secreted into gut also contribute to self-digestion
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57
Q

What putrefaction

A

=putrification
Digestion of proteins and tissues by anaerobic bacteria

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58
Q

Describe the process of putrefaction

A
  • as proteins break down, gases are produced and excreted by anaerobic bacteria (causing a putrid odor)
  • gases diffuse to other parts of the body, leading to bloating of torso then limbs
  • increased pressure weakens and seperates tissues
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59
Q

What factors effect decomposition rate

A
  • weather, exposure, humidity
    = encourages bacteria
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60
Q

How does mummification work?

A
  • remove organs
  • dry body with salt for 30 days
  • wash body cavity with wine and spices
  • wrap body in antrimicrobial bandages
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61
Q

What are plant cell walls made of?

A
  • cellulose (B1-4 glucose)
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62
Q

What is the fungal cell wall

A

Chitin

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63
Q

What bacterial cell wall

A
  • peptidoglycan

(Polysaccharides held together by oligopeptide crosslinks)

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64
Q

What is oligopeptide

A
  • small peptide 2-20 amino acids
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65
Q

How many types of bacterial cell walls are there and how are they distinguished?

A
  • two
  • gram staining
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66
Q

How is gram positive bacteria identified?

A
  • crystal violet CV+ ions stain
  • Blue-violet colour
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67
Q

How are gram negative bacteria’s identified

A
  • do not turn blue violet
  • absorb the pink counter stain safranin
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68
Q

Label this cell wall

A

Gram-positive bacterial cell wall

1 - peptidoglycan
2 - teichoic acid
3 - integral protein
4 - transmembrane protein
5 - cell membrane
6 - cell wall
7 - surface protein

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69
Q

Label this bacterial cell wall

A

1 - lipopolysaccharides
2 - periplasmic space
3 - peptidoglycan
4 - outer membrane proteins
5/6 - membrane proteins
7- cell membrane
8 - cell wall
9 - outer membrane
10- porins

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70
Q

What do porins do?

A
  • allows water and hydrophilic things into the bacteria
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71
Q

Describe the structure of a gram positive bacterial cell

A
  • thick layer of peptidoglycan
  • one cell membrane
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72
Q

Describe the structure of a negative bacterial cell wall

A
  • thin layer of peptidoglycan
  • cell membrane and another outer cell membrane
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73
Q

Describe the process of bacterial cell walls being stained

A
  • crystal violet ions enter cell walls and gram negative outer membrane
  • I- ions bind to and fix CV+ ions
  • decolouriser disrupts gram negative outer membrane and so CV+I- is lost
  • counter stain adds pink colour which allows us to visualise decolourised cells
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74
Q

Summarise gram+ bacteria

A
  • blue violet stain due to CV
  • more susceptible lysozyme and antibodies
  • tend to live on skin
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75
Q

Summarise gram negative bacteria

A
  • pink stain due to safranin
  • tend to live in wet areas because are susceptible to drying out
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76
Q

How do bacteria reproduce?

A
  • asexual reproduction by binary fission
  • this is vertical gene transfer
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77
Q

How can bacteria obtain foreign DNA?

A

(And therefore obtains genetic variation)
Via horizontal gene transfer

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78
Q

Give the three methods of horizontal gene transfer

A
  1. Transformation
  2. Transduction (via bacteriophage)
  3. Conjugation (via pillus)
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79
Q

Describe transformation

A
  • DNA is taken up from environment and may be integrated into bacterial DNA
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80
Q

Describe transduction

A
  • bacterial DNA transferred to other bacteria by bacteriophages
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81
Q

Describe conjugation

A
  • DNA passed through cytoplasm in pilus to another bacteria cell
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82
Q

What are two ways that bacteria causes illness

A
  • produces endotoxins
  • releases exotoxins
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83
Q

Describe endotoxins

A
  • in outer layer of Gram-negative cells
  • causes vomiting diarrhoea, fever
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84
Q

Describe exotoxins

A
  • soluble proteins released in metabolism
  • toxic effect on cells, inhibit neurotransmitters
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85
Q

What is a virus

A
  • submicroscopic infectious agents that replicate inside living cells
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86
Q

What are viral particles called?

A

Virons

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87
Q

Why are viruses not considered living?

A
  • non-cellular
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88
Q

How large are viruses?

A
  • 0.02-0.3um (20-300nm)
  • 50x smaller than average bacterium
  • many morphologies
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89
Q

What is the protein coat made of?

A
  • capsid
  • repeating protein units (capsomeres)
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90
Q

Describe viruses genome

A
  • RNA or DNA
  • single or double stranded
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91
Q

Describe viruses genetic material;

A
  • linear or circular
  • in segments or not
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92
Q

What are the 4 general morphologies

A
  1. Helical
  2. Polyhedral
  3. Enveloped
  4. Complex
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93
Q

Give an example of a helical structure

A
  • Tobacco mosaic virus (TMV)
  • infects tobacco plants and other members of the plant family solanaceae
  • first virus to be identified
  • RNA is bound to the protein helix by interactions between negative RNA and positive proteins
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94
Q

Give an example of a polyhedral virus

A
  • Adenovirus
  • causes a variety of illness (colds or UTIs)
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95
Q

Describe enveloped viruses

A
  • influenza/ COVID 19/HIV
  • surround themselves in host cell membrane (can be outer or internal membranes (ER))
  • the membrane is studded with viral proteins made by the host cell
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96
Q

What are bacteriophages

A
  • complex structure
  • several structure

E.g
- polyhedral head bound to a helical tail with protruding protein tail fibres
- acts as a molecular syringe attaching to a bacterial host and injecting the viral genome into the bacterial cell

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97
Q

Describe the bacteriophage life cycle

A
  1. Attach to host bacterium
  2. Phage DNA enters and destroys bacterial DNA
  3. Viral genome and proteins assembled
  4. New bacteriophages synthesise
  5. Released as cell lyses
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98
Q

What is the lytic cycle

A
  • production of new viruses
  • destruction of host cell
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99
Q

What is the lysogenic cycle

A
  • integration of viral genome
  • viral genome replicated
  • can switch to the lurid cycle
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100
Q

Bacteriophages can have either a ……. Cycle

A
  • lytic cycle
  • lysogenic cycle
  • or both
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101
Q

Lytic phases break open…

A

Immediately after replication of the virion

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102
Q

Describe lysogenic phages

A
  • viral genome integrates into host dna and replicates with it harmlessly (may become a plasmid)
  • virus remains dormant until host conditions deteriorate; phages become active
  • reproductive cycle is initiated in lysis of the host cell
  • the lysogenic cycle allows the host cell to continue to survive and reproduce, the virus is reproduced in all of the cells offspring
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103
Q

What is a latency period in viruses

A
  • in latency these viruses exist in nervous tissue for a long time without producing new visions
  • leave latency periodically and has effects when virus replicates
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104
Q

Describe the influenza virus life cycle

A
  1. Absorption off docking to host receptor protein
  2. Entry into host cytoplasm
  3. Synthesis of viral components using host cell machinery
  4. Assembly of new viruses
  5. Budding from host cell
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105
Q

Describe the retrovirus life cycle (e.g HIV)

A
  • rna is first transcribed into DNA
    (Influenza rna is used directly in protein synthesis)
  • retroviruses insert new DNA into host DNA (influenza does not insert genetic material into host DNA)
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106
Q

How do viruses cause illness?

A
  • destruction of host cell during lysis
  • hijack host cells protein synthesis to slow down host cells metabolism
  • produce toxins
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107
Q

How are bacteria and viruses transmitted

A

Person to person spread
- skin to skin
- maternal infection
- blood to blood
- sexually transmitted
- stool to mouth
- droplet transmission

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108
Q

How are bacteria and viruses transmitted

A

Person to person spread
- skin to skin
- maternal infection
- blood to blood
- sexually transmitted
- stool to mouth
- droplet transmission

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109
Q

What is an immune system

A
  • a host defence system compromising of many biological structures and processes that protect against disease
110
Q

The immune system detects:

A
  • a wide variety of pathogen (viruses to parasitic worms)
  • distinguishes them from the organisms own tissue
111
Q

What are the two major subsystems of the immune system?

A
  • the innate (non specific)
  • the adaptive (specific)
112
Q

Both sub-systems use:

A
  • humoral immunity
  • cell mediated immunity
113
Q

What are the three components of the innate subsystem?

A
  • anatomical
  • humoral
  • cell mediated
114
Q

What are the two components of the adaptive immune system?

A
  • humoral
  • cell mediated
115
Q

What is the definition of humoral?

A

Molecules that circulate in the blood

116
Q

What is the definition of cell mediated?

A
  • cell to cell contact
117
Q

Describe the specificity of the innate IS

A
  • non antigen specific v
118
Q

Describe the time take for a response in the innate IS?

A
  • immediate maximum
119
Q

Are memory cells made in the non-specific IS?

A

No

120
Q

Describe the specificity of the adaptive IS?

A
  • antigen specific
121
Q

How long does it take for the adaptive IS to generate a response?

A
  • lag time between exposure and maximum response
122
Q

Are memory cells made in the specific immune system?

A

Yes

123
Q

What are the cells involved in the specific IS?

A

Lymphocytes
- T cells
- B cells

124
Q

What are the cells involved in the non specific IS?

A
  • phagocytes
  • auxiliary cells
125
Q

What makes up anatomical immunity in the non-specific IS?

A
  • physical factors
  • biological factors
  • chemical factors
126
Q

What makes up humoral immunity in the non-specific IS?

A
  • complement
  • cytokines
  • coagulation
127
Q

What makes up cell mediated immunity?

A
  • phagocytosis
  • inflammation
128
Q

Describe the anatomical barriers in the mouth, nose and eyes?

A

Chemical
- saliva
- tears
- mucus
- lysozyme

129
Q

Name the physical barrier in the airways

A

Ciliated cells

130
Q

How does the gut microbiome act as an anatomical barrier

A

Biological
- good bacteria outcompetes bad bacteria

131
Q

Describe the skins anatomical barriers

A
  • chemical: sebum
  • physical: keratin (makes skin waterproof)
  • biological: microbiome
132
Q

What is keratin?

A
  • fibrous structural protein
  • hair, nails, outer layer
  • protects epithelial cells from damage or stress
133
Q

What makes keratin so strong and insoluble

A
  • many disulphide bridges
134
Q

What is cornification?

A
  • the process of forming a physical barrier of stratified squamous epithelial tissue
135
Q

Skin surface epithelial cells stop …………………………………… and are almost completely filled by ………………………..

A
  • metabolic reactions
  • keratin
  • eventually the nucleus and organelles disappear and cells undergo programmed death as they become fully keratinised
136
Q

How is the cornified layer or epidermis thickened?

A
  • rubbing and pressure
  • turns into protective calluses
  • keratinised epidermal cells are constantly shed and replaced
137
Q

What is a lysosome?

A
  • enzyme that cleaves bonds in peptidoglycan
  • leads to lysis of bacterial cells
138
Q

Where is lysozyme found?

A
  • tears, saliva, human milk and mucus
  • present in macrophages and neutrophils
  • conjunctiva
139
Q

How does lysozyme cause losing of bacterial cells

A

Through osmotic shock
- lysozyme hydrolyses beta 1,4 glycosidic bonds in peptidoglycan (major component in gram + bacterial cell walls)

140
Q

What is osmotic shock?

A
  • sudden change in osmotic pressure
141
Q

What is the complement system?

A
  • enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells
  • promotes inflammation
  • disrupts pathogen cell membrane
142
Q

What does the complement system consist of?

A
  • more than 30 small proteins that are synthesised mainly by hepatocytes in the liver, but also by macrophages, monocytes and some epithelial cells
143
Q

Complement proteins circulate…

A
  • in blood as inactive precursors
  • activated when needed
144
Q

Describe the four processes of the complement system

A
  • lysis
  • chemotaxis
  • opsonisation
  • inflammation
145
Q

What is lysis?

A
  • binding to and lysing target cells
146
Q

What is chemotoxis?

A
  • attraction of phagocytes to the site of infection
147
Q

What is opsonisation?

A
  • opsonise (mark) bacteria for digestion by phagocytes
148
Q

Describe the process of inflammation?

A
  • stimulates mast cells to release histamine
149
Q

What are cytokines?

A
  • group of small proteins that initiate changes in gene expression
150
Q

What are cytokines produced by

A

Many cell types
- macrophages
- b lymphocytes
- t lymphocytes
- mast cells
- endothelial cell

151
Q

How are changes in gene expression and transcription factors triggered

A
  • each cytokine has a complementary cell-surface receptor
  • binding to the receptor
152
Q

How is cytokine storm syndrome triggered?

A
  • over-secretion of cytokines
153
Q

What is an interferon?

A
  • produced by virus infected cells
  • induces virus resistance in uninfected cells
154
Q

What is part of the innate humoral response?

A
  • complement
  • cytokines
  • blood clotting proteins
155
Q

What is part of the innate cell mediated response?

A
  • mast cells and histamine inflammation
  • phagocytosis
156
Q

How do mast cells respond to bacterial invasion?

A
  • releasing histamine leading to inflammation
157
Q

Describe the changes histamine causes

A
  1. Vasodilation -> increased blood supply (redness + heat)
  2. Increased vascular permeability (endothelial cells contract) -> swelling (oedema) and pain
  3. More WBCs arrive to clear bacteria
158
Q

What is phagocytosis?

A
  • engulf and digest pathogens
159
Q

Name the different types of phagocytic cells

A
  • neutrophils
  • monocytes + macrophages
160
Q

Describe neutrophils

A
  • multilobed nucleus
  • produce free radicals (nitric acid and super oxide) to break down bacterial DNA and protein
  • activate specific (adaptive) IS
161
Q

Describe monocytes and macrophages

A
  • bean shaped nucleus
  • circulate in blood as antigens + mature into macrophages when they move into tissues
  • present monocytes to activate adaptive immune system
162
Q

Describe the process of phagocytosis

A
  1. Movement towards bacteria by chemotaxis
  2. Bind to bacterium
  3. Engulf bacterium
  4. Phagosome formation
  5. Phagosome and lysosomes fuse
  6. Digestion of bacterium by lysosome enzymes/ destruction with super oxide
  7. Egestion of bacterial debris
  8. Antigen presentation (monocytes and macrophages only)
163
Q

How do monocytes and macrophages present antigens?

A
  • with a major histocompatibility complex (MHC) on cell membrane
  • role = presentation of processed antigen
164
Q

What destroys parasites?

A
  • eosinophils
165
Q

What destroys infected cells?

A
  • natural killer cells
166
Q

What causes allergic reactions?

A
  • basophils
167
Q

What cells make up the humoral component of the specific IS

A

B cells

168
Q

What cells make up the cell mediated component of the specific IS

A
  • T cells
169
Q

What are B cells?

A

B lymphocytes
- mature in bone marrow
- circulate in blood and lymphatic system

170
Q

What is the BCR?

A

B cell receptor
- surface receptor for specific antigen

171
Q

What are antibodies?

A
  • soluble version of BCR
  • specific for same antigen
172
Q

What is responsible for antigen presentation in B cells?

A

MHC molecule

173
Q

Structure of a B cell

A
174
Q

What are antigens:?

A

antibody generating
- any substance that can be specifically recognised by B cells and/or T cells
- usually organic molecules, proteins, glycoproteins or polysaccharides
- free or bound to pathogens
- native or processed

175
Q

What does it mean when an antigen is native?

A
  • not yet processed
176
Q

What does it means when an antigen is processed?

A
  • partly digested and presented on an APC
177
Q

What are antibodies?

A
  • immunoglobulins Ig
  • V shaped
  • 2 identical light pp chain and 2 identical long pp chains held together by disulphide bridges
  • constant regions + variable regions (for antigen bindings)
  • each antibody specific for one antigen
178
Q

What are the four different roles of antibodies?

A
  • opsonisation
  • complement activation
  • agglunation
  • neutralisation
179
Q

What is the BCR?

A

B cell receptor
- membrane-bound version of antibody
- has signal transaction functional area
- recognises antigen and initiates response in B cell

180
Q

What is the MHC?

A
  • major histocompatibilty complex
  • presentation of processed antigen
181
Q

How are T cell-independent B cells activated?-

A
  • antigen binding triggers developing of memory + plasma cells
182
Q

How are T cell-dependent B cells activated?

A
  • antigens binding to B cells leads to antigen presentation by B cell
  • T helper cell binds to antigens presented by B cell
  • activated T helper cell releases cytokines
  • cytokines stimulate B cell to develop into plasma and memory cells
183
Q

Are memory B cells long or short lived

A

Long

184
Q

Are plasma cells long or short lived

A

Short

185
Q

Selective B cell activation leads to…

A
  • clonal expansion and maturation
186
Q

Describe the primary immune response

A
  • time lag
  • long lasting immunity
  • fewer antibodies
187
Q

Describe the secondary immune response

A
  • immediate
  • short lasting (booster)
  • more antibodies
188
Q

Compare how plasma cells are formed from T cell-in/dependent B cells

A

Independent
- 2nd antigen exposure (activated -> memory -> plasma)

Dependent
- B cell presents antigens and is now an APC
- T helper cell binds to presented antigen through complementary CD4 receptor
- cytokines released
- plasma cell or memory cell

189
Q

Describe T cells

A
  • lymphocytes
  • mature in thymus
  • circulate in blood and lymphatic system
  • differentiate into 4 types
190
Q

What are the 4 types of T cells

A
  • helper
  • killer
  • memory
  • suppressor

Have T cell receptor on surface

191
Q

Describe the T cell receptor

A
  • recognises processed antigen bound to MHC
  • antigen binding to TCR triggers activation of T cell
  • co-receptor
192
Q

What does T cell activation lead to

A
  • differentiation
  • clonal expansion
193
Q

What is the role of t helper cells?

A
  • b cell activation
  • phagocyte enhancement (by opsonisation of microbes)
  • t killer cell activation
194
Q

What is the role of t killer cells

A
  • destruction of virus infected cells
195
Q

Describe the function of T killer cells

A
  • infected body cell
  • antigen presentation
  • t killer cell binds to antigen (TKC activated)
  • T helper cell releases cytokines for maturation
  • t killer cells release perforin
  • pores formed in infected cell -> water enters and cell lyses
196
Q

Describe the steps of clonal selection and expansion of T cells

A
  • selection + activation
  • maturation + expansion
197
Q

What is tuberculosis?

A
  • infectious disease of the respiratory system
  • caused by Mycobacterium tuberculosis
198
Q

What is the first phase of TB?

A

Primary/latent infection
- may not have any symptoms
- 4-6 weeks

199
Q

What is the second phase of TB

A

Active tuberculosis
- symptoms
- last years

200
Q

Describe the first phase of TB

A
  • M tuberculosis bacteria reach alveolia and cause inflammatory response
  • macrophages ingest bacteria, but cannot digest them due to very resistant waxy capsule
  • bacteria can reproduce or become dormant inside macrophages
  • groups of infected and uninfected macrophages, and B and T cells aggregate to form a granuloma
  • granuloma becomes encapsulated forming a tubercle
  • inside is starved of oxygen killing tb bacteria and macrophages
  • infection is often fought off and lung tissue heals
201
Q

How does MT evade the immune system

A
  • MT taken up by phagocytosis cannot be destroyed due to their thick waxy capusle
  • TB bacteria can survive inside macrophages and lie dormant for years
  • reactivation can occur at later point
202
Q

Why does the second phase occur?

A
  • first phase cannot be contained (too many bacteria)
  • reactivation of latent bacteria if immune system is weakened
203
Q

How is tuberculosis transmitted

A
  • only transmitted by people with active tb
  • via coughing sneezing etc.
  • inhaled bacteria reaching lungs may cause infection
  • highly contagious
204
Q

When might the immune system be weakened?

A
  • the old and the young
  • when a person is malnourished
  • when a person has HIV or AIDS
205
Q

What happens in the lung during active TB?

A
  • rapid mutation of bacteria
  • destruction of lung tissue (holes appear)
206
Q

What are the other parts of the body that TB can affect?

A
  • glands (glandular TB)
  • bones
  • CNS
207
Q

What ate the symptoms of TB?

A
  • coughing (including coughing up blood)
  • shortness of breath
  • loss of appetite and weight loss
  • fever and night sweats
  • fatigue
208
Q

How is fever initiated?

A
  • inflammatory response: neutrophils and macrophages release interleukin 1
  • IL-1 causes hypothalamus to release prostaglandin
  • prostaglandin resets the hypothalamic thermostat to new higher body temperature
  • nerve impulse activate body effectors leading to increase of body temperature
209
Q

What body effectors being activated lead to an increase of body temperature

A
  • shivering
  • higher metabolic rate
  • inhibition of sweating
  • inhibition of vasodilation
210
Q

How does fever aid immune response?

A
  • increase phagocytosis
  • increasing number of T cells
  • decreasing reproduction of pathogens
211
Q

How can you test for TB

A

Skin test
- injection of antigen (tuberculin)
- if antibodies present, inflammation occurs
-> shows antibodies present

212
Q

What might cause false results using a skin test?

A
  • positive: vaccinated
  • negative: disease latent
213
Q

What do blood tests test for in TB

A
  • test for presence of TB antigen specific T-cells
214
Q

How do you analyse TB for bacteria?

A
  • sputum coughed up is tested for bacteria species
  • cell wall stain
  • DNA analysis
215
Q

How do you treat and control TB?

A
  • antibiotics (streptomycin for 6 months, usually other antibiotics too)
  • improve living standards to control transmission
  • screening by X-ray
  • BCG vaccine
216
Q

How do you treat and control TB?

A
  • antibiotics (streptomycin for 6 months, usually other antibiotics too)
  • improve living standards to control transmission
  • screening by X-ray
  • BCG vaccine
217
Q

What is HIV?

A
  • human immunodeficieny virus
  • virus causing AIDS
  • targets T helper cells
218
Q

What is AIDS?

A
  • acquired immune deficiency syndrome
  • disease of the human immune system
  • increases susceptibility to other dieseases
219
Q

How is HIV transmitted?

A
  • unprotected sex with infected partner
  • sharing needles with infected person
  • transmission from infected mother to fetus
  • infection from blood transfusions
220
Q

What is the structure of the HIV virus?

A
  • retrovirus
  • spherical, diameter ~120nm
  • 2 copies of ssRNA with 9 genes
221
Q

Label this diagram of HIV

A
222
Q

Describe the HIV life cycle

A
  1. HIV gp120 docking protein binds to CD4 co-receptor on T helper cells (and macrophages which express low levels of CD4)
    - HIV fuses with cell membrane and release SSRNA into host cell
  2. Reverse transcriptase copies viral ssRNA to make dsDNA
  3. Viral DNA is transported into nucleus
    - integrase inserts viral DNA into host DNA
  4. Transcription and translation of viral envelope protein gp160
    - transcription of viral DNA into RNA to be used as a new virus genome
    - translation of RNA to make new viral polyprotein
  5. Viral envelope protein gp160 passes through secretory pathway where it is cleaved to form gp120 + gp41
  6. Viral envelope proteins are incorporated into host cell membrane
  7. New viral RNA and polyprotein move to cell surface and new immature HIV virion forms by budding from cell membrane
  8. Virus matures when HIV protease cleaves individual HIV proteins and enzymes from polyprotein
    - virus is now infectious
223
Q

Describe the course of HIV

A

Acute phase -> latent phase -> disease phase (AIDS)

224
Q

Describe the stages of AIDs

A

Acute phase -> latent phase -> disease phase

225
Q

What does AIDs development depend on?

A
  • genetic response to infection
  • immune response to initial infection
  • lifestyle and nutrition
  • availability of ART drugs
226
Q

Describe the acute phase of AIDS

A

2-6 weeks post infection:
- possible influenza like symptoms
- rapid replication of virus
- rapid loss of T-helper cells
3-12 weeks post infection
- antibodies appear in blood
8-12 weeks post infection
- infected Th cells recognised and destroyed by T-killer cells

227
Q

Describe the latent phase of AIDs

A

12 weeks to several years:
- provirus (viral DNA) dormant in Th cells recognised genome
- virus reproduces slowly
- immune system controls infection
- no symptoms but increasing tendency to suffer infections
- possible reactivation of dormant diseases (e.g TB)

228
Q

What is the disease phase of HIV and AIDS?

A
  • rapid decline of Th cells
  • rapid increase in viral load
  • HIV-related symptoms appear (weight loss, fatigue, diarrhoea, sweats)
  • later stages: major weight loss, dementia, cancer
  • increase risk of opportunistic infections
229
Q

How are t helper cells killed?

A
  • non-permissive infected Th cells killed so incomplete reverse transcripts trigger immune response
  • permissive infected Th cells killed by virus production (5% of Th cells)
230
Q

What is the effect of killing t helper cells?

A
  • no b cell activation
  • no phagocyte enhancement
  • no t killer cell activation
231
Q

What are the type of HIV drugs?

A
  • fusion inhibitors
  • reverse transcriptase inhibitions
  • integrase inhibitions
  • gp120-CD4 binding inhibitors
  • protease inhibitors
232
Q

What is PrEP

A

Pre-exposure prophylaxis
- use of ART in anticipation of potential HIV exposure with the aim of preventing trnasmission
- works to keep virus from establishing a permanent infection

233
Q

What is the process of transcription

A
  • copying of DNA code into mRNA
  • occurs in the nucleus
  • catalysed by RNA polymerase
234
Q

What is transcription initiation?

A
  • rna polymerase binds to the promoter
  • rna polymerase unwinds DNA double helix in preparation for transcription
235
Q

What is transcription elongation

A
  • RNA polymerase transcribes the antisense (template) strand into RNA sequence (via complementary base pairing using free RNA nucleotides + DNA sequences as template)
  • rna polymerase uses U instead of T
  • RNA polymerase joins nucleotides with phosphodiester bonds
  • ## RNA polymerase synthesis in 5’ -> 3’ direction
236
Q

Describe transcription termination

A
  • where RNA polymerase reaches the terminator transcription stops
  • RNA polymerase/ RNA/ DNA complex disassembles
237
Q

Where does post-transcription modification of RNA take place?

A
  • occurs in the nucleus
238
Q

What is 5’ capping?

A
  • an altered guanine is added to the 5’ end of the RNA at start of transcription
  • the 5’ cap provides resistance to 5’ exonucleuases which cleave nucleotides from the ends of RNA
239
Q

What is 3’ polyadenylation

A
  • a poly A tail resists degradation of the 3’ end of the RNA in the cytoplasm
  • these adenines are gradually lost in the cytoplasm and then the whole RNA is degraded when no longer needed
240
Q

What is RNA splicing?

A
  • splicing is the removal of introns
241
Q

What is alternative splicing?

A
  • allows different proteins to be produced when different exons are spliced together
242
Q

What is translocation of mRNA

A
  • the transport of mRNA out of the nucleus via nuclear pores
243
Q

What is genetic code

A
  • sequence of bases in DNA is translated into the sequence of amino acids in a protein
244
Q

What is degenerate?

A
  • amino acids can be coded for by more than 1 codon
245
Q

What are the three 3 stop codons

A

TAA, TAG, TGA

246
Q

How is an amino acid loaded onto tRNA?

A
  • using tRNA synthetase
  • forming aminoacyl-tRNA
247
Q

Label this ribosome

A

1 - large ribosomal subunit
2 - small ribosomal subunit
3 - E-site (exit)
4 - P site (peptidyl tRNA)
5 - A site (aminoacyl tRNA)
6 - mRNA binding site

248
Q

Describe translation initiation

A
  • small ribosomal subunit with Met-tRNA in P-site moves along mRNA to find first AUG
  • when first AUG is found, large subunit of ribosome binds
  • next aminoacyl-tRNA moves into position
249
Q

Describe translation elongation

A
  • aminoacyl-tRNA corresponding to next A-site binds to P site of ribosome
  • the 2 amino acids are joined by a peptide bonds (via peptide synthetase)
  • ribosome moves on to next codon release first tRNA, second tRNA moves to the codon
  • amino acrylic-tRNA corresponding to the next codon binds to the A-site
  • repeats until stop codon reached and a release factor is loaded into A site
  • peptide chain is release and ribosome complex seperates
250
Q

What are polysomes

A
  • several ribosomes can bind to the same RNA thus synthesising several polypeptide chains at the same time
251
Q

What is immunity

A
  • having sufficient B and T memory cells to avoid disease
252
Q

What is active immunity?

A
  • exposure to antigen
  • antibody production
  • memory cells made
253
Q

What is passive immunity?

A
  • antibodies received
  • no memory cells made
254
Q

What is in a vaccine

A
  • live, attenuated (weakened) pathogen
  • dead pathogen
  • antigen of pathogen
  • related organism with similar antigens
  • toxoids (modified, harmless toxins)
255
Q

How do vaccines work?

A
  • weakened pathogen injected
  • immune response 1 takes place, memory cells made
256
Q

What are booster injections?

A

= re exposure to antigen
- increases number of B and T memory cells to maintain protective levels

257
Q

What is herd immunity

A

When a high enough portion of the population is vaccinated to also protect those without immunity

258
Q

Why is there no HIV vaccine

A
  • difficulty in producing a vaccine
  • virus mutates frequently giving rise to virus subtypes
259
Q

What are the risks of vaccination?

A
  • pain at site of injection
  • fever/ feeling unwell
  • severe side effects
260
Q

What is bacteriostatic antibiotic?

A

= prevents multiplication (hosts immune system can then destroy pathogen)
- target protein synthesis
- target dna replication
- target RNA transcription

261
Q

What is bactericidal antibiotic

A

=kill bacteria via cell lysis
- target bacterial cell membrane
- target bacterial cell wall
- interfere with enzyme activity

262
Q

Why do we still have diseases like TB, AIDs

A
  • a mutation in the pathogen may help the microbe to evade the IS
  • evolutionary race between pathogen and immune system
263
Q

Why do we still have genetic diseases

A
  • heterozygous advantage
264
Q

What is antigenic drift?

A
  • changes in drift due to mutation in pathogen
265
Q

What is antigenic shift?

A
  • a change in shift due to mixing of antigene from several species
266
Q

How does TB evade the immune system

A
  • resistant to digestion by lysosomes enzymes
  • can survive inside macrophages
  • can destroy macrophages and infect others
267
Q

how does HIV evade the immune system

A
  • antigenic drift and shift
  • hiv infects t helper cells
    -> lies dormant
    -> kills t helper cells
268
Q

How does antibiotic resistance arise?

A

Due to mutations
- alter antibiotic
- degrade antibiotic
- pump out antibiotic

Due to horizontal gene transfer via plasmids

269
Q

What is MDR TB

A

Multi drug resistant TB
- resistant to two most powerful TB frontline antibiotics

270
Q

What is XDR TB

A

= MDR TB that has also become resistant to secret-line antibiotics

271
Q

What strategies reduce prevalence of HealthCare Associated Infections?

A
  • better hygiene
  • fewer antibiotics used (only when bacterial infection confirmed)
  • isolation of infected patients

Biology (6 decks)

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