Immunity and forensics Flashcards
Describe the structure of a virus
- nucleic acid - DNA or RNA inside
- surrounded by a capsid (protein coat)
- attachment proteins
- proteins in capsids - eg enzymes like reverse transcriptase.
Describe the structure of a bacterium
- Cell wall and cell membrane
- Plasmids and free floating DNA
- smaller ribosomes than eukaryotes.
- flagella (some)
- Pilli
- slime capsule
Describe How HIV would enter, then exit from a host cell.
- attaches to receptors on lymphocyte/host cell.
- injects RNA into host cell.
- Uses host cell resources to replicate itself
- cell becomes saturated and copies of HIV leave the cell, killing it (Lysis)
Name some entry routes of pathogens
- breaks in skin
- mucosal surfaces
- Respiratory system
- Digestive system
What are physical non-specific defenses against pathogens?
- Skin: physical barrier and sebum. Also has bacterial coating which can out-compete pathogens that are no adapted to skin conditions.
- cillia: digestive and respiratory systems
- gut and genital flora: bacteria
- enzymes in tears and saliva (Lysozyme) - causes pathogens to lyse.
What are some non-specific immune responses?
- inflammation
- interferons
- phagocytosis
- gut and skin flora
Explain how inflammation occurs.
- histamines released by mast cells.
- causes vasodilation, increasing blood flow to the area. (red appearance)
- increases permeability of capillaries: increases water in the area (swelling)
Describe 3 ways in which interferons act.
- increase non-specific immune response
- inhibit production of viral proteins.
- activate WBCs to specific immune response.
What are interferons?
Anti-viral proteins that prevent viruses from spreading to uninfected cells.
Describe the stages of phagocytosis
- Pathogen is ingulfed by phagocyte.
- it then gets enclosed in a vesicle, called a phagosome.
- Phagosome then binds to a lysosome, hydrolysing the pathogen. (formed a phagolysosome)
- phagocyte will then present the pathogen’s antigens on its surface, meaning it has become an APC.
Describe the structure of an antibody.
- light chain (short) (top)
- heavy chain (long) (bottom)
- antigen binding site (variable with different antibodies)
- Constant region (not variable, the same for all antibodies)
- Hinge region - gives flexibility to bind to an antigen at different angles.
Describe what is meant by splicing
- Introns (non-coding) are ‘cut out’ from pre-RNA, then exons are rearranged by spliceosomes in different combinations to form mature functional RNA.
Describe the stages of the cell-mediated response
- T cells look for non-self antigens, triggering clonal selection.
- they mature inside the thymus
- they then divide through mitosis - (clonal expansion)
- they can either give rise to Killer, Helper or memory T cells
- Helper T cells: produce cytokines to attract Macrophages and B cells to the area.
- Killer T cells: bind to receptors on infected cell, puncture holes and release toxins to destroy infected cells (lysis)
- Memory T cells: stay behind to remember the pathogen, allowing for a faster immune response upon reinfection.
Describe the humorol response.
- Involves B cell responses
- mature in bone marrow
- clonal selection and clonal expansion
- 2 types: plasma and memory (can arise during expansion)
- Plasma cells: produce antibodies, and therefore have plenty of mitochondria and ReR. This causes agglutination, causing immobility of pathogens and an inability to reproduce, attracting macrophages and neutrophils to the area to destroy the pathogens.
- Memory cells: stay behind, faster response upon re-infection because of remembering the pathogen.
Explain how changes in the blood vessels result in the redness and swelling seen at the site
of inflammation.
- histamines are released
- leads to vasodilation, resulting in redness in the area due to more blood flow to the area.
- Swelling caused by capillaries becoming more permeable, allowing plasma fluid to flood the area.
Describe how HIV particles are able to enter T helper cells
- Attach to CD4 receptor protein on surface of T helper cell
- injects viral RNA into T helper cell through viral envelope fusing with cell membrane of T helper cell.
Explain why the destruction of T helper cells causes the symptoms of AIDS.
- reduces cytokine production
- so less B cells are activated, producing less antibodies against HIV
- increasing risk of opportunistic infections.
Explain why the presence of microorganisms on the skin and in the gut helps to
prevent pathogenic organisms multiplying in the body
- bacteria on skin and in gut more well-adapted to conditions
- so bacteria on skin and gut out-competes pathogenic organisms for resources
- bacteria in the gut secrete lactic acid which also destroys pathogens.
A small number of people have been identified who are resistant to HIV.
They have a mutation in a gene coding for a protein in the cell membrane.
(i) Deduce why this mutation makes these people resistant to HIV infection
- glycoprotein unable to bind to receptor on host cell.
- meaning that viral RNA cannot enter the cell.
Stem cell therapy can be used to treat patients infected with HIV.
The bone marrow of these patients can be destroyed using radiotherapy.
The patients can then be given stem cells from the bone marrow of a donor who has this
mutation.
Explain why these stem cells may prevent HIV causing AIDS.
- stem cells can differentiate into specialised cells.
- so they differentiate into T cells that have the mutated gene
- so mutated CD4 prevents HIV entering the T cell
- prevents destruction of T cells, so HIV virus doesn’t stay in blood.