B5 Flashcards

(57 cards)

1
Q

process of immune response

A
  • phagocytes engulf pathogen
  • phagocytes display antigens
  • complementary T lymphocytes bind to antigen
    –> stimulates phagocytes, TH cells which stimulate B lymphocytes, cytotoxic T cells, T memory cells
  • B lymphocytes
  • englulf pathogens (not phagocytosis)
  • displays antigen on the surface
  • TH cell binds to antigen
  • stim. B lymphocytes to divide
    –> memory B cells, plasma cells
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2
Q

describe how vaccination can lead to protection against x

A
  • the antigen of x binds to the surface receptor on a specific B cell
  • T cells stimulate the activation and division of B cells
  • activated B cells divide by mitosis- clonal selection
  • B cells produce plasma cells which release antibodies
  • some B cells become memory cells
  • memory cells produce more antibodies faster
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3
Q

how does a vaccine lead to the production of antibodies against a disease causing organism

A
  • vaccine contains antigen from pathogen
  • macrophage englufs antigen and presents it on its cell-surface membrane
  • T-cell with complementary receptor site binds to the antigen
  • T-cell becomes activated and stimulates the mitotic division of B cells with the complementary antibody on their surface
  • B cells divide by mitosis to form a clone of plasma cells that produce the same antibodies
  • and form memory B cells that produce the same antibodies faster
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4
Q

active vs passive immunity

A
  • active involves MEMORY cells ; passive does not
  • active involves the production of antibodies by plasma/ memory cells ; passive involves the antibody being introduced to the body from an outside source
  • active = long term, antibody produced in response to antigen ; passive = short term, antibody given = broken down
  • active can take time to develop ; passive = fast acting
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5
Q

describe how HIV = replicated

A
  • attachment proteins attach to CD4 receptors on helper T cells
  • HIV nucleic acid/ RNA enters TH cell
  • reverse transcriptase converts RNA –> DNA
  • viral protein = produced
  • virus particles = assembled and released from cell
  • the HIV particles break away from the TH cell with a piece of its cell surface membrane surrounding them–> forms lipid envelope.

if longer answer:
- RNA –> DNA using reverse transcriptase
- DNA = inserted into TH cell DNA
- DNA transcribed into HIV mRNA
- HIV mRNA translated into new HIV proteins
—> for assembly into viral particles

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6
Q

describe how a phagocyte destroys a pathogen present in its blood

A
  • engulfs pathogen
  • forms a vesicle (phagosome)
  • lysosome fuses with vesicle
  • enzymes (lysozymes) hydrolyse the pathogen
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7
Q

what is the role of the disulfide bridge in forming the quaternary structure of an antibody?

A
  • joins 2 different polypeptides
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8
Q

explain how HIV affects the production of antibodies when AIDS develops in a person

A
  • less antibody produced
  • HIV destroys helper T cell
  • so fewer B cells activated
  • fewer differentiate into plasma cells
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9
Q

suggest and explain how viruses can develop to infect other species

A
  • mutation in the viral DNA
  • altered tertiary structure of the viral attachment protein
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10
Q

describe how the B lymphocytes respond to vaccination- do not include details of the cellular response

A
  • B lymphocyte antibody from plasma cells binds to complementary receptor/ antigen
  • B cell divides by mitosis
  • plasma cells release monoclonal antibodies
  • B- lymphocytes produce memory cells
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11
Q

what is a monoclonal antibody?

A

antibodies with the SAME TERTIARY STRUCTURE

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12
Q

describe the role of antibodies in producing a positive result in an ELISA test

A

1st antibody binds to complementary antigen
2nd antibody w/ enzyme attached = added
2nd antibody attaches to 1st antibody
substrate solution added –> colour changes

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13
Q

describe and explain the role of antibodies in stimulating phagocytosis. do not include details of phagocytosis

A

bind to antigen
- cause AGGLUTINATION

are markers
- attract PHAGOCYTES

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14
Q

explain how treatment with antivenom works and why it is essential to use passive immunity rather than active

A

antivenom antibodies bind to the antigen and destroy it
active immunity would be too slow

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15
Q

a mixture of venoms from several snakes of the same species are used in one antivenom. explain why

A
  • may be different form of antigen/ toxin within a species
  • different antibodies are complementary to different antigens
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16
Q

suggest and explain why AZT does not destroy HIV in the body, but stops/ slows the development of AIDS

A
  • person infected with HIV has HIV DNA in their DNA
  • new HIV particles = still made
  • AZT inhibits reverse transcriptase
  • AZT stops the HIV particles forming new HIV DNA
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17
Q

describe how phagocytosis of a virus leads to the presentation of its antigens

A
  • phagosome fuses with lysosome
  • virus = destroyed by hydrolytic enzymes / lysozymes
  • antigens from virus = displayed on cell membrane
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18
Q

describe how presentation of a virus antigen leads to the secretion of an antibody against the virus antigen

A

TH cell binds to antigen on the phagocyte
- this TH cell stimulates specific B cell
- B cell clones –> plasma cells

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19
Q

what is an antigen

A

foreign protein that stimulates an immune response

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20
Q

what is an antibody

A

a protein specific to antigen produced by B cells

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21
Q

the body’s defence mechanisms can be specific or non-specific
- describe difference
- examples

A

specific:
- slower response
- specific for each pathogen
e.g. cell mediated, T lymph ; humoral, B lymph

non-specific:
- immediate response
- same for all pathogens
e.g. physical barrier, phagocytosis

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22
Q

what are foreign cells that the immune system needs to identify

A
  • pathogens e.g. HIV
  • non-self material e.g. cells from other organisms of same species
  • toxins e.g. those produced by bacteria
  • abnormal body cells e.g cancer cells
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23
Q

how does the body distinguish between self and non self cells

A
  • each type of cell has specific proteins on its surface
  • proteins have a huge variety of specific tertiary structures
24
Q

problem with non-self cells and tissue/ organ transplants

A
  • the immune system recognises the cells as non-self
  • it therefore attempts to destroy the transplant
  • to minimise the effect of rejection, donor tissues are normally matched as closely as possible e.g. genetically close relatives
  • immunosupressant drugs are also administered to reduce the level of the immune response
25
what is clonal selection and why is it necessary
- specific lymphocytes are not produced in response to an infection- they already exist - there is a high probability that, when a pathogen enters the body, there will be a lymphocyte with a protein on its surface complementary to one of the proteins on the pathogen so the lymphocyte will 'recognise' the pathogen - when an infection occurs, the one type already present is stimulated to divide by mitosis to build up its numbers to a level where it can be effective in destroying it --> this is CLONAL SELECTION * this explains why there is a TIME LAG between exposure to the pathogen and the body's defences bringing it under control.
26
how lymphocytes recognise cells belonging to the body
- in the fetus, lymphocytes are constantly colliding with other cells - infection in the fetus is rare because it is protected by the mother and placenta - lymphocytes will therefore only collide with self cells - some lymphocytes will have receptors that are complementary to the self cells - these lymphocytes die/ are suppressed - the only remaining lymphocytes are those that fit foreign material - in adults, lymphocytes produced in bone marrow initially only encounter self antigens - any lymphocytes that show an immune response to these self antigens undergo programmed cell death (apoptosis) before they can differentiate into mature lymphocytes NO CLONES of these anti-self lymphocytes will appear in the blood, leaving only those that may respond to non-self
27
process of phagocytosis
non-specific - chemical products of pathogens/ dead or abnormal cells act as attractants, causing phagocytes to move towards the pathogen ---> follows a chemical concentration gradient by chemotaxis - phagocytes have several receptors on their cell surface membrane that recognise and attach to chemicals on the pathogen surface - they engulf the pathogen to form a phagosome vesicle - lysosomes move towards the vesicle and fuse with it - hydrolytic enzymes (lysozymes) destroy ingested bacteria by hydrolysis of their cell walls - the hydrolysis products are either discarded, absorbed by the phagocyte cytoplasm or are DISPLAYED on the cell-surface membrane (stimulates T-LYMPHOCYTES) phagocytes have a multi-lobated nucleus --> to squeeze between cells
28
the process of cell-mediated immunity
- the primary immune response
29
what is immunity
the ability of organisms to resist infection by protecting against disease-causing microorganisms or the toxins that invade their bodies
30
what are lymphocytes - T - B
type of WBC responsible for specific immune response T produced by stem cells in bone marrow mature in thymus (T) gland associated with CELL MEDIATED immunity B mature in bone (B) marrow associated with HUMORAL immunity --> immunity involving antibodies that are present in bodily fluids e.g. blood plasma
31
examples of APCs recognised by the RECEPTORS on T cells
- phagocytes that have engulfed + hydrolysed a pathogen which present some of its antigens on their own cell surface membrane - body cells invaded by a virus that present some viral antigens on their cell surface membrane - transplanted cells from individuals of the same species have different antigens on their cell surface membrane - cancer cells are different from normal body cells and present antigens on their cell surface membranes.
32
the stages of the cell mediated response
- pathogens invade body cells/engulfed by phagocytes - the phagocyte places antigens from the pathogen on its cell surface membrane - receptors on a specific helper T cell fit exactly onto these antigens - this attachment activates the T cell to divide rapidly by mitosis to form a clone --> clonal selection *the cloned T cells:* - develop into memory t cells ---> recognise specific antigen at second infection - so can divide to form clones of the original cell ----> form cytotoxic, phagocytes to kill pathogen - stimulate phagocytes to engulf pathogens by phagocytosis - form helper T cells which stimulate B lymohocytes to divide and secrete their antibody - activate cytotoxic T cells
33
how cytotoxic t cells kill infected cells
- produce protein called perforin - makes holes in cell-surface membrane - cell membrane becomes freely permeable to all substances, cell dies as result - the action of T cells is most effective against viruses because viruses replicate inside cells - as viruses use living cells to replicate, this sacrifice of body cells prevents viruses multiplying and infecting more cells
34
process of humoral immunity
primary immune response - involves antibodies which are soluble in the blood and tissue fluid - when e.g. an antigen (a protein on the surface of the pathogen, foreign cell, toxin, damaged or abnormal cell) enters the blood or tissue fluid, there will be one B cell that has the antibody on its surface whose shape is complementary to the antigen - the antibody therefore attaches to the complementary antigen - the antigen enters the B lymphocyte by endocytosis and is presented on its on its cell surface membrane - TH cells bind to these processed antigens and stimulate this B cell to divide by mitosis to form a clone of identical B cells in clonal selection, all of which produce the antibody that is specific to the foreign antigen- they are MONOCLONAL antibodies - some pathogens also produce toxins, each toxin molecule can also act as an antigen in each clone, the cells produced develop into one of two types of clone: PLASMA CELLS: secrete antibodies into blood plasma - these cells survive only for a few days, but each can make around 2000 antibodies every second - these antibodies lead to the destruction of the antigen - the plasma cells are therefore responsible for the immediate response of the body against infection MEMORY CELLS: responsible for the SECONDARY immune response - live considerably longer than plasma cells, often for decades - these cells do not produce antibodies directly, but circulate in the blood and tissue fluid - when they encounter the same antigen at a later date, they divide rapidly and differentiate into plasma cells and more memory cells - the plasma cells produce the antibodies needed to destroy the pathogen, while new memory cells circulate in readiness for any future infection - in this way * 1. the surface antigens of an invading pathogen are taken up by a B cell 2. the B cell processes the antigens and presents them on its surface 3. TH cells (specific, activated t lymphocytes) attach to the processed antigen on the B cell, activating the B cell 4. the B cell is now activated to divide by mitosis to give a clone of plasma cells in clonal selection 5. the cloned plasma cells produce and secrete the specific antibody that fits the antigen on the pathogen surface (PRIMARY IMMUNE response) 6. the antibody attaches to the antigens on the pathogen and destroys them 7. some b cells differentiate into memory cells. these can respond to future infections by the same pathogen by dividing rapidly and developing into plasma cells that produce antibodies --> this is the SECONDARY IMMUNE response
35
structure of an antibody
- made of 4 polypeptide chains - chains of one pair are long : heavy chains - chains of other pair are shorter : light chains - each antibody has a specific binding site that fits exactly onto a specific antigen ---> forms an ANTIGEN-ANTIBODY COMPLEX - the binding site is different on different antibodies --> VARIABLE REGION - each binding site consists of a sequence of amino acids that form a specific 3D shape that binds directly to a specific antigen - the rest of the antibody = CONSTANT REGION - this binds onto receptors on cells such as B CELLS
36
how the antibody leads to the destruction of the antigen
- do not destroy antigen directly, but prepares for destruction cause AGGLUTINATION - binds to antigen - easier for phagocytes to locate as thy are less spread out in body serve as MARKERS - stimulate phagocytes to engulf the bacterial cells to which they are attached
37
uses of monoclonal antibodies
*targeting medication to specific cell types by attaching a therapeutic drug to an antibody - monoclonal antibodies are produced that are specific to antigens on cancer cells --> must have specific, non-self antigen - these antibodies are given to a patient and attach themselves to the receptors on their cancer cells - they attach to the surface of their cancer cells and block the chemical signals that stimulate their uncontrolled growth - also act as marker for phagocytosis *indirect monoclonal antibody therapy - attaching a radioactive/ cytotoxic drug to the monoclonal antibody - when the antibody attaches to the cancer cells it kills them *medical diagnosis - bind to specific chemical/ antigen - can measure level of certain chemical in blood *pregnancy testing - placenta produces HCG - monoclonal antibodies on the test strip of a home pregnancy test are linked to coloured particles - if HCG is present in the urine, it binds to these antibodies - the HCG-antibody-colour complex moves along the strip until it is trapped by a different antibody, creating a coloured line
38
ethical use of monoclonal antibodies
- The development of monoclonal antibodies has provided society with the power and opportunity to treat diseases in new ways. However, with this power and opportunity comes responsibility. The use of monoclonal antibodies raises some ethical issues. - Production of monoclonal antibodies involves the use of mice. - These mice are used to produce both antibodies and tumour cells. - The production of tumour cells involves deliberately inducing cancer in mice. - Despite the specific guidelines drawn up to minimise any suffering, some people still have reservations about using animals in this way. Monoclonal antibodies have been used successfully to treat a number of diseases, including cancer and diabetes, saving many lives. - There have also been some deaths associated with their use in the treatment of multiple sclerosis. - It is important that patients have full knowledge of the risks and benefits of these drugs before giving permission for them to be used (=informed consent). - Testing for the safety of new drugs presents certain dangers. In 2006, six healthy volunteers took part in the trial of a new monoclonal antibody in London. Within minutes they suffered multiple organ failure, probably as a result of T cells overproducing chemicals that stimulate an immune response or attacking the body tissues. We therefore must balance the advantages that a new medicine provides with the dangers that its use might bring. Only then can we make informed decisions at individual, local, national and global levels about the ethical use of drugs such as monoclonal antibodies.
39
some antigens found on the surface of tumour cells are also found on the surface of healthy human cells. why do tumour treatments often cause side effects?
- monoclonal antibody will bind to healthy cells - causes death/ damage to healthy cells
40
active vs passive immunity
ACTIVE produced by stimulating the production of antibodies in the individual's own immune system - direct contact with the pathogen/ antigen is necessary -immunity takes time to develop - it is generally longer lasting and is of two types; *NATURAL ACTIVE: results from individual becoming infected with a disease under normal circumstances. the body produces its own antibodies and may continue to do so for years *ARTIFICIAL ACTIVE: basis of vaccination. involves inducing an immune response in an individual, without them suffering symptoms. PASSIVE produced by the introduction of antibodies from an outside source - no direct contact with pathogen necessary - immunity is acquired immediately - as the antibodies are not being produced by the individuals, they are not replaced when broken down, no memory cells = formed so no long lasting immunity *NATURAL PASSIVE: antibodies enter in natural method e.g. placenta *ARTIFICIAL PASSIVE: antibodies injected into body
41
vaccination
- Vaccination is the introduction of the appropriate disease antigens into the body, either by injection or by mouth. The intention is to simulate a PRIMARY immune response against a particular disease. - The material introduced is called a vaccine and, in whatever form, it contains one or more types of antigen from the pathogen. - These antigens stimulate the immune response. - The response is slight because only a small amount of antigen has been introduced. - However, the crucial factor is that memory cells are produced - These remain in the blood and allow a greater, and more immediate, response to a future infection with the pathogen. - The result is that there is a rapid production of antibodies and the new infection is rapidly overcome before it can cause any harm and with few, if any, symptoms. --> memory b cells remain in blood, when encounter pathogen again, undergo a QUICKER SECONDARY IMMUNE RESPONSE - When carried out on a large scale, this provides protection against disease not only for individuals, but also for whole populations.
42
features of a successful vaccination programme
o Must be economically available in sufficient quantities to immunise most of the vulnerable population. o There must be few side effects from vaccination. Unpleasant side-effects may discourage individuals from being vaccinated o Means of producing, storing and transporting the vaccine must be available. This may include advanced equipment, hygienic conditions and refrigerated transport. o There must be the means of administering the vaccine properly at an appropriate time. This involves training staff with appropriate skills at different centres throughout the population. o It must be possible to vaccinate the vast majority of the vulnerable population to produce herd immunity.
43
herd immunity
- Herd immunity arises when a sufficiently large proportion of the population has been vaccinated to make it difficult for a pathogen to spread within that population - The concept is based on the idea that pathogens are passed between individuals in close contact - Where the vast majority of the population is immune, it is highly improbable that a susceptible individual will come in contact with an infected person. - In this way, those individuals who are not immune to the disease are nevertheless protected. - Herd immunity is important because it is never possible to vaccinate everyone in a large population. - For example, babies, and very young children are not vaccinated because their immune system is not yet fully functional - It could also be dangerous to vaccinate those who are ill or who have compromised immune systems. - The percentage of the population that must be vaccinated to achieve herd immunity is different for each disease, - To achieve herd immunity, vaccination is best carried out at one time. This means that, for a certain period, there are very few individuals in the population with the disease and the transmission of the pathogen is interrupted
44
why a vaccination may not eliminate a disease
Even when these criteria for successful vaccination are met, it can still prove extremely difficult to eradicate a disease. The reasons are: - Vaccination fails to induce immunity in certain individuals for example in those who are immunosuppressed. - Individuals may develop the disease immediately after vaccination but before their immunity levels are high enough to prevent it. (in the time lag before developing antibodies) - The pathogen may mutate frequently, so that its antigens change suddenly. This means that vaccines suddenly become ineffective because the new antigens on the pathogen are no longer recognised by the immune system. o As a result, the immune system does not produce the antibodies to destroy the pathogen. o This is ANTIGENIC VARIABILITY, and happens e.g. with the influenzas virus o Immunity is therefore short-lived and individuals may develop repeat bouts during their lifetime. - There may be many varieties of a pathogen that it is almost impossible to develop a vaccine that is effective against them all. - Certain pathogens ‘hide’ from the body’s immune system, either by concealing themselves inside cells, or by living in places out of reach, such as within the intestines. - Individuals may have objections to vaccinations for religious, medical or ethical reasons.
45
ethics of using vaccines
- Vaccinations have saved millions of lives - However they do raise ethical issues * - The production and use of vaccines raises the following concerns: - the use of animals in production/development - balancing the risks of possibly long-term side effects against the risk of developing a disease that causes even greater harm. - On whom the vaccines should be tested, how tests should be carried out, to what extent individuals should be asked to accept the risk in the interest of public health. - Is it acceptable to trial a new vaccine with unknown health risks only in a country where the targeted disease is common, on the basis that the population there has the most to gain if it proves successful? - To be fully effective, should vaccination be compulsory? Can people opt out (on medical/religious/ethical basis)? - Should expensive vaccination programmes continue when a disease is almost eradicated, even though this might mean less money for the treatment of other diseases? - How can any individual health risks from vaccines be balanced against the advantages of controlling a disease for the benefit of the whole population?
46
when making monoclonal antibodies using an animal, why should they be monitored
- so animal doesnt suffer from the toxin - so they don't suffer anaemia as a result of blood collection - so the animal does not have pathogen that could be transferred to humans
47
vaccine 1 : smal vol. antigen vaccine 2 :larger vol. antigen why?
primary immune response: - B cells specific to the venom reproduce by mitosis in clonal selectgion - B cells produce plasma cells and memory cells ---> plasma cells release antibodies secondary: - the 2nd dose produces antibodies in higher concentration and more quickly (memory cells stimulated)
48
structure of HIV
lipid envelope with embedded attachment proteins matrix capsid, enclosing 2 single RNA strands, reverse transcriptase
49
role of reversed transcriptase
catalyses production of DNA from RNA makes HIV a RETROVIRUS
50
how HIV causes AIDS symptoms
- Specifically attacks T-helper cells. o This kills them/interferes with their normal function Uninfected person has 800-1200 helper T cells per mm^3 blood o In AIDS patients, an reach 200 per mm^3 - Helper T cells are essential in cell mediated immunity - Without a sufficient number of them, the immune system cannot stimulate B-cells to produce antibodies or the cytotoxic T cells that kill cells infected with pathogens. - Memory cells may also become infected and destroyed - As a result, the body is unable to produce an adequate immune response and becomes susceptible to other infections and cancers. o Also leads to weight loss and diarrhoea - eventually causes death. - HIV does not kill individuals directly. It prevents the immune system from functioning normally so that it becomes susceptible to other pathogens, which causes death * * - susceptible to other pathogens - pathogens reproduce and cause disease in host - damages cells/tissues/organs/ released toxins
51
once infected with HIV...
a person = HIV positive -the replication of HIV often goes into dormancy and only recommences, leading to AIDS, many years later
52
when do people with HIV develop AIDS
- when the TH cell numbers in their body reach a critically low level
53
REPLICATION OF HIV
- attachment proteins attach to the receptors on the TH cell - nucleic acid/ RNA enters TH cell - reverse transcriptase converts RNA -DNA - DNA inserted into TH DNA - viral protein produced: transcribed viral mRNA, translated mRNA protein - viral particles = assembled and released from cell using cell membrane as lipid envelope
54
what is the ELISA test and how does it work
enzyme linked immunosorbent assay - uses antibodies to detect presence and quantity of protein in a sample 1. Apply the sample to a surface e.g. a slide, on which the protein in the sample (e.g. antigens) will attach. 2. Wash the surface repeatedly to remove unattached antigens. 3. Add the antibody specific to the antigen, leave to bind 4. Wash the surface to remove excess antibody. 5. Add a 2nd antibody that binds with the 1st. a. This 2nd antibody has an enzyme attached. 6. Add the colourless substrate of the enzyme 7. The enzyme changes the substrate to a coloured product 8. The amount of the antigen present is proportional to the intensity of the colour. ELISA= important mostly for detecting quantity, as many drugs are normally present in the blood in small amounts.
55
why are antibiotics ineffective against viruses
1 role of antibiotics is preventing bacteria from making normal cell walls. - In bacterial cells (like plant cells) water constantly enters by osmosis. - The entry of water would normally cause the cell to burst o This doesn’t happen due to the cell wall, made from MUREIN (peptidoglycan) which is tough and not easily stretched. - As water enters, the cell expands and pushes against the cell wall. o The wall resists expansion so stops further influx of water - Antibiotics inhibit certain enzymes required for the synthesis and assembly of peptide cross-linkages in bacterial cell walls. o The cell wall is therefore weakened and so the cell bursts BY OSMOTIC LYSIS - Viruses rely on host cells- they lack their own metabolic pathways and structures. - So antibiotics are ineffective as there are no metabolic mechanisms / cell structures to disrupt. - Viruses also have a protein coat, not a murein cell wall so there are no sites for antibiotics to work. - animal cells do not have a cell wall so are UNAFFECTED by antibiotics
56
determining the genome of a virus could allow scientists to develop a vaccine. describe how
could identify proteins then identify potential antigens
57