T6 - Infection, immunity and forensics Flashcards

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1
Q

What is autolysis

A
  • The breakdown of the body’s own tissues due to the action of the body’s own enzymes.
  • Digestive enzymes of the gut and hydrolytic enzymes of the cells lysosomes hydrolyse the body tissues following death.
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2
Q

How to determine the time of death of a mammal

A
  1. The extent of decomposition
  2. Stage of succession
  3. Forensic entomology
  4. Body temperature
  5. Degree of muscle contraction
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3
Q

How is the extent of decomposition used to determine TOD

A
  • Digestive enzymes begin to break down the surrounding tissue.
  • How much a body has decayed can be used to determine how long it has been dead for.
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4
Q

How is the stage of succession used to determine TOD

A
  • As the body decays the species colonising the body change.
  • Analysis of the community of species present can be used to determine TOD.
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5
Q

How is forensic entomology used to determine TOD

A
  • Study of insects e.g. maggots
  • Determining the age of insects present can be used to find TOD.
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6
Q

How is body temperature used to determine TOD

A
  • Body temperature falls until ambient temperature is reached (algor mortis)
  • As heat-producing metabolic reactions stop
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7
Q

How is the degree of muscle contraction used to determine TOD

A
  • Rigor mortis occurs 3 hours after death and only lasts 36 hours
  • No ATP so muscles begin to stiffen
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8
Q

What goes into a PCR mixture

A
  1. DNA sample
  2. DNA primers
  3. DNA polymerase
  4. Free DNA mono-nucleotides
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9
Q

What are the 4 steps in PCR

A
  1. The temperature is raised to 90°C to separate the DNA strands called denaturation.
  2. The temperature is lowered to 55°C to allow primers to bind to a specific sequence on the DNA sample called annealing.
  3. The temperature is raised to 70°C to allow DNA polymerase to replicate the strands by complementary base pairing of the free DNA nucleotides to the DNA template strands called elongation.
  4. This temperature cycle is repeated many times.
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10
Q

How is DNA profiling using gel electrophoresis done

A
  1. Use the restriction enzyme endonuclease to create fragments of DNA, fragments vary in size because of short tandem repeats (STR).
  2. The fragments are put into wells in a gel called agarose.
  3. An electronic current is applied, so the negatively charged DNA fragments move towards the anode (because of phosphate groups).
  4. Shorter fragments travel through the gel at a faster rate than longer fragments.
  5. Florescent tags are added to make the bands of DNA fragments visible.
  6. Observe the bands from two samples to see if they are the same pattern or different.
  7. Gel electrophoresis creates a unique individual pattern.
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11
Q

Difference between bacteria and viruses

A
  1. Bacteria have circular DNA but viruses have linear DNA or RNA.
  2. Bacteria do not require a host to survive but viruses need a host to survive.
  3. Viruses are smaller than bacteria
  4. Bacteria have cell membrane, ribosomes, plasmids, flagellum and other organelles that viruses do not have.
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12
Q

How can HIV be transmitted

A
  1. Sexual intercourse
  2. Blood donation
  3. Sharing needles
  4. Mother to child across the placenta
  5. Mother to child through breast milk
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13
Q

How does HIV replicate

A
  1. HIV binds to T-helper cells, the GP120 binds to the CD4 receptor on T-helper cells. And merge together by endocytosis.
  2. The capsid breaks down and the enzymes and RNA are released into the T-helper cell.
  3. Enzyme reverse transcriptase transcribes the viral RNA to viral DNA using free DNA nucleotides found in the host cell. Single-stranded DNA is made into double-stranded DNA.
  4. Enzyme integrase then adds the viral DNA to the hosts DNA.
  5. The host cell’s enzymes then produce copies of viral components as the viral DNA gets transcribed, which are assembled to form new viruses.
  6. New HIV exit the host cell by exocytosis and enter the blood, where they can infect other T-helper cells and repeat the process. Host cells can also lyse/burst.
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14
Q

How does HIV turn into AIDS

A
  1. Initially cause fevers and headaches.
  2. Latency period where replication rate drops.
  3. Weakened immune system leading to AIDS.
  4. Opportunistic infections, such as TB, which can lead to death.
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15
Q

2 ways to stop HIV

A
  1. Stop HIV entering the host cell
    - Drugs could bind to receptors on HIV (GP120) blocking the binding site.
    - Drugs can bind to CD4 receptors on T-helper cells preventing GP120 from binding.
  2. Stop the merging of viral and host DNA
    - Inhibiting reverse transcriptase
    - Integrase could be inhibited
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16
Q

How is TB spread

A
  1. Mycobacterium tuberculosis enters the air in tiny droplets of liquid released from the lungs. Through coughing or sneezing.
  2. TB is transmitted when uninfected people inhale these droplets. Faster in crowded areas.
  3. Once inside the lungs, TB bacteria are engulfed by phagocytes.
  4. The bacteria may be able to survive and reproduce while inside phagocytes.
  5. Over time the infected phagocytes will become encased in structures called tubercles in the lungs where the bacteria will remain dormant.
  6. The bacteria can become activated and over power the immune system at a later stage (during HIV infection). Known as the active phase of TB.
  7. Symptoms include - fever, fatigue, coughing and lung inflammation.
  8. If left untreated it can lead to respiratory failure and spread to other parts of the body leading to organ failure.
17
Q

Why can’t TB in tubercles be destroyed

A

Tubercles are covered with a tick waxy coat preventing them from being destroyed.

18
Q

Describe the process of phagocytosis

A
  1. Chemicals released by the pathogen cause the phagocyte (e.g. macrophage or neutrophil) to move towards it.
  2. Receptors on the cell-surface membrane of a phagocyte binds to an antigen on a pathogen, which is recognised as non-self.
  3. The phagocyte’s cell-surface membrane engulf the pathogen, taking it in to form a phagosome.
  4. Lysosomes fuse with the phagosome where lysozyme hydrolyses the pathogen.
  5. Macrophages present antigens of the pathogen on the cell-surface membrane becoming an antigen-presenting cell (APC).
  6. Using molecules called the major histocompatibility complex (MHC).
19
Q

How do lysozymes fight against bacteria

A
  • Lysozymes hydrolyse peptidoglycan (murein) in bacterial cell wall
  • Causing bacteria to lyse/burst
20
Q

How do interferons fight against viruses

A
  • Interferons are secreted by cells invaded by viruses
  • Interferons bind to receptors on the surface membrane of uninfected cells
  • Preventing viral replication
21
Q

Examples of active immunity

A
  1. Active natural - infection
  2. Active artificial - vaccination
22
Q

Examples of passive immunity

A
  1. Passive natural - maternal antibodies
  2. Passive artificial - monoclonal antibodies
23
Q

How do vaccines prevent future infections

A
  • Vaccines activate the bodies primary response by causing the body to produce memory cells.
  • Memory cells remain in the body for a long time and provide protection upon re-infection this is the secondary immune response.
  • Resulting in the production of antibodies to be faster.
24
Q

What are the 2 types of antibiotics

A
  1. Bactericidal - kills bacteria by destroying cell wall, causing them to lyse.
  2. Bacteriostatic - inhibits the replication of bacteria cells by stopping protein synthesis.
25
Q

How do T-helper cells get activated

A
  1. They get activated when they bind to an antigen presenting cell e.g. a macrophage
  2. The T-helper cell’s CD4+ receptor binds to the MHC on the APC.
  3. Then T-helper cell undergoes clonal selection to become active T-helper cells and memory T-helper cells.
  4. The active T-helper cells then bind to the antigen on the APC to release cytokines which attract macrophages and T-killer cells to the antigen.
  5. Also activating B cells.
26
Q

How do T-killer cells get activated

A
  1. A T-killer cell, with a specific complementary receptor, binds to a specific antigen on the surface of an APC e.g. macrophage / infected cell.
  2. The binding to the antigen activates the T-killer cell, causing it to undergo clonal selection to produce large numbers of identical T-killer cells.
  3. Cloned T-killer cells bind to the antigen upon infected cells and release chemicals (e.g. perforin) that punctures the cell membrane leading to cell lysis.
  4. During clonal selection, some cloned T-killer cells remain in the immune system as T-killer memory cells.
27
Q

How do B-cells get activated

A
  1. The cytokines released from the T-helper cells stimulate the B-cells into clonal selection
  2. B-cell differentiate into plasma cells and B-memory cells.
28
Q

How do B-cells get activated

A
  1. The cytokines released from the T-helper cells stimulate the B-cells into clonal selection
  2. B-cell differentiate into plasma cells and B-memory cells.
29
Q

What is opsonisation

A

Antibodies coat microbes and mark them for phagocytes.