a2 immunity Flashcards

(49 cards)

1
Q

why are viruses not considered cells?

A

as they have no cytoplasm, cell membrane etc…

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2
Q

why are viruses not considered living organisms

A

as they have no metabolism and can only reproduce inside host cells and their replication depends on metabolism of host cells

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3
Q

describe structure of viruses

A

1- strand of linear DNA or RNA
2-protein coat called capsid made of capsomeres
3-external envelope made of lipids and proteins
4-surface proteins that are complementary on surface proteins on host cells and bind to them helping virus enter host cell

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4
Q

how to produce new viral particles

A

1- replication; the genetic material of viruses replicate inside host cells
2-protein synthesis; the virus uses host cell energy, enzymes and nucleotides to form mrna , then mrna is incorporated into host cell ribosomes where its translated to form protein coat
3-assembly; the new genetic material is incorporated into new protein coat forming large numbers of viral particles, they cause lysis of infected cells and burst out of the cells infecting nearby cells

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5
Q

describe mechanism of infection of virus

A

1-the viral surface proteins bind to a specific type of receptor on host cell surface
2- the virus injects its core (DNA\rna + or - enzymes
that’s why each virus only binds to a specific type of cells
eg; influenza virus only binds to respiratory cells and not digestive system cells

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6
Q

describe lysogenic pathway

A

1-in DNA viruses; the viral DNA is incorporated into DNA of host cell using viral integrase enzyme
2- in RNA enzymes; an RNA strand is used as a template to synthesize DNA this process is called reverse transcription and is catalyzed by the enzyme reverse transcriptase then the viral DNA is incorporated into DNA of host cell using viral integrase enzyme
- the viral genetic material only replicates with replication of host cells - the viral stays dormant inside the cell not causing any symptoms
-a virus may suddenly shift from lysogenic to lytic pathway

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7
Q

how do antiviral drugs slow down lysis process

A

1- they block receptors of host cells so viral particles cannot bind
2-so the virus cant inject its core into the host cell and cant replicate itself
3-this prevents lysis of host cells
-some antivirals work by blocking enzymes responsible for its replication

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8
Q

what are the routes of infection of diseases

A

1-broken skin barrier
2-openings of the body (mouth, eyes etc.)
3- bacteria flora may turn pathogenic

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9
Q

what are patterns of disease spread

A

1-endemic; disease spread at constant low rate in a certain area
2-epidemic; widespread of disease at a high rate to nearby areas
3-pandemic; worldwide spread of disease

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10
Q

what are the modes of infection

A

1-inhalation (airborne); coughing or sneezing from an infected person , droplets containing pathogens are inhaled by a healthy person
2-ingestion; of contaminated foods or drinks which causes diseases such as salmonella
3-vectors; living organisms transmit diseases from an infected person to a healthy person such as mosquitos with malaria
4- fomites; objects that carry infections such as hospital towels or bedding and blood transfusion or sharing needles
5- direct contact; such as spread of skin infections and sexually transmitted disease such as gonorrhea

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11
Q

what’s the difference between non specific immune mechanisms and specific immune response

A

non specific doesn’t depend on a specific type of pathogens and doesn’t change with repeated infections while specific depends on a specific type of pathogens and improves with repeated infections

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12
Q

state and explain physical barriers to infection

A

1-intact skin; it consists of keratin which is an indigestible protein that acts as a barrier and prevents entry of pathogens
2- bacteria flora; is a harmless normal bacteria which outcompetes pathogenic bacteria for space and nutrition and may release chemicals which make medium unsuitable for pathogenic bacteria and they also may destroy them
3- lysozymes ; they digest bacterial cell wall killing pathogenic bacteria, they are secreted by skin in sebum, lacrimal glands in eyes, respiratory epithelium and phagocytes
4-respiratory epithelium; contains mucus which traps pathogens and cilia which wafts this mucus away to the throat
5-stomach; contains -stomach acid which kills bacteria -bacteria flora which outcompetes pathogenic bacteria for space and nutrition -pepsin which digests proteins -anaerobic conditions which kill aerobic bacteria

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13
Q

state and explain how inflammation happens

A

entry of a pathogen or a foreign body causes mast cells to rupture (more blood) releasing a chemical called histamine which acts as a local vasodilator which allows more blood containing phagocytes that engulf bacteria to flow into arterioles and increases permeability of capillaries

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14
Q

what are the characteristics of inflammation

A

1- redness (due to vasodilation as there’s more blood)
2- hotness (better enzymatic activity)
3-oedema (swelling)

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15
Q

how does a fever happen

A

1-the body’s immune response to infection may lead to fever
2-pathogens cant enter the brain as they cannot pass the blood brain barrier, however they release toxins that are small enough to pass which may affect the thermoregulatory center of the hypothalamus affecting heat loss mechanisms

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16
Q

what is the importance of fever

A

1-temperature higher than 37 degrees is not optimum for pathogens so it may denature their enzymes or destroy them
2-our immune systems activity is better at higher temperature

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17
Q

what are the hazards of fever

A

1- if temperature exceeds a certain limit our enzymes may denature
2-excessive sweating may cause dehydration and loss of important ions

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18
Q

what is the simplified mechanism of pathogens

A

1-they engulf bacteria
2-they digest it using hydrolytic enzymes
3-they destroy it

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19
Q

define MHC

A

glycoprotein receptors on the surface of the body cells that can be recognized by the immune system as self (they are unique for each person)

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20
Q

define foreign antigen

A

glycoprotein on the surface of pathogens that can be recognized by the immune system as non-self

21
Q

what are antibodies and their function

A

1-they are proteins produced by plasma cells
2-they are complementary to foreign antigens
3-they bind to antigens forming antigen-antibody complexes

22
Q

describe the structure of antibodies

A

they consist of 4 polypeptide chains;
1- 2 heavy chains joined together by disulfide bonds
2- 2 light chains
- constant regions are made up of heavy chains only
-variable regions are made up of both heavy and light chains

23
Q

what is the mechanism of antibodies

A

-they bind to antigens forming antigen-antibody complex
1- agglutination (immobilization and clumping) : they clump together for easy phagocytosis
2-opsonization (marking) : attracting phagocytes for faster phagocytosis
3- toxic neutralization; they bind to toxins of bacteria neutralizing them

23
Q

how does t helper cell activation occur

A

-t helper cell activation must occur before antibody mediated or cell mediated immune response
1-macrophages engulf bacteria and secrete lysozymes to digest it
2-they extract the antibody (processing) to be displayed on the MHC of macrophages
3-the macrophage now becomes an antigen presenting cell
4- T helper cells with CD-4 receptors bind to antigens on MHC of macrophages
5- then they divide by mitosis into effector t helper cells and memory t helper cells

24
how does the humoral immune response occur
1- B cells with complementary receptors bind to specific pathogen antigens 2- B cells display the antigens over their MHC (antigen presentation) 3- active T helper cells; -active t helper cells with complementary CD 4 receptors are chosen, they bind to antigens present on B cells MHC -they release cytokines 4-cytokines; they stimulate B cells to divide by mitosis into effector B cells and memory B cells 5- effector B cells are not immediately effective they first differentiate into plasma cells 6-plasma cells secrete antibodies complementary to the foreign antigen 7-the antibodies cause agglutination (clumping), opsonization (marking) and toxic neutralization to enhance phagocytes 8-finally the pathogens are digested and destroyed by enhanced phagocytosis
25
how does cell mediated immune response occur
1-infected host cell displays viral antigen on its MHC 2- T killer cells with specific CD 4 receptors bind to the viral antigens 3- active T helper cells release cytokines 4-cytokines simulate T killer cells to divide by mitosis into effector T killer and memory T killer 5- effector T killer cells release a chemical called perforin 6-this chemical causes lysis of infected host cells releasing viral particles to be accessible to antibodies 7-antibodies cause agglutination and opsonization so viral particles are digested and destroyed by enhanced phagocytosis
26
when are memory cells formed and when do they preform their function
they are formed in primary immune response and they work in secondary immune response
27
what is the role of T helper cells in specific immune response
-they release cytokines which are needed for; 1-clone proliferation of B cells to be differentiated into plasma cells and release antibodies 2-clone proliferation of T killer cells that secrete perforin - T helper cells are responsible for activation of the immune system
28
what is interferon and how does it work
its a chemical secreted by virus infected host cells that stops viral replication by; 1-inhibiting protein synthesis so viruses cant synthesize protein coat 2-increases antigen presentation on MHC of host cells so more T killers are activated 3-promotes inflammation so more T killers are brought to the site of infection
29
what are the limitations of vaccine
1-antigenic variation; a pathogen undergoes a mutation which changes the shape of its active site 2-antigenic concealment; a pathogen hides the shape of its antigen by having a slime coat or bacteria inside cells 3-some vaccines require special storage conditions
30
what's meant by opportunistic infection
an infection that only produces symptoms in people suffering from immune suppression and take advantage of weak immunity and trigger other opportunistic infections such as TB
31
describe fate of TB
- the TB may be completely destroyed by the phagocyte -some bacteria may evade digestion by releasing substances that prevent fusion of lysosome and phagosome - the bacteria survive and replicate inside phagocytes -the immune system seals off infected phagocytes forming tubercles -the bacteria inside tubercles becomes dormant and shows no symptoms -dormant bacteria may become reactivated forming tb -reactivation is triggered by weak immune system
32
what are symptoms of TB
1-wasting of the body 2-low grade fever 3-night sweats 4-coughing with blood tinged sputum
33
what are complications of TB
1- serious erosion of lung tissue 2-erosion of blood vessels causing bleeding 3-bacteria might enter eroded blood vessels moving to other organs causing organ failure 4- TB may cause other opportunistic infections
34
how to diagnose TB
1- chest X-ray 2- sputum culture analysis 3- bacterial DNA analysis
35
how to treat TB and why
combination of antibiotics (as if bacteria is resistant to one type of antibiotics it will be sensitive for others) for a long period of time (long enough time to kill all bacteria)
36
how to prevent and control TB
1- improving the standards of living in areas with low socioeconomic status 2-avoid over-crowdedness and ensure good ventilation 3-avoid drinking unpasteurized milk 4- administer BCG vaccine to -healthcare workers, -infants under the age of 40 days, -travelers to areas with high prevalence of TB
37
state reasons for decrease or increase of TB
decrease; 1-BCG vaccine 2-multidrug use 3-X-ray screening increase; 1-appearance of multidrug resistant strains 2-globalisation of travel and immigration 3-deterioration of standards of living
38
structure of HIV
1- 2 strands of RNA 2- has viral envelope (phospholipid bilayer) 3- has protein coat (capsid) 4- contains enzymes such as reverse transcriptase and integrase 5-has GP 120 and GP 41 antigens
39
explain why HIV is an immunodeficiency virus
-as it destroys immune system -by attacking T helper cells -preventing activation of B/ T killer cells -so fewer antibodies produced
40
what are the modes of transmission of AIDS
-sexual contact -blood transmission such as sharing needles -maternal relationship
41
how to treat HIV
use antiviral agents such as azathioprine -antiviral drugs that treat HIV aim at coating GP 120 or blocking CD4 receptors which only slows down replication
42
what are limitations of treatment of AIDS
-its a virus so antibiotics are not effective -its constantly and rapidly mutating so developing a drug is difficult -it doesn't infect animals so trials of safety and efficacy are very difficult -difficult to diagnose as it has non characteristic symptoms
43
how to prevent AIDS
-sterilize surgical and dental equipment -careful screening of donated blood -promote safe sex by physical barriers such as condoms -avoid having multiple sexual partners -screening of high risk groups -avoid sharing needles
44
what are the limitations of prevention of AIDS
-symptomless carriers can infect others -known carriers may hide the fact due to social stigma -vaccination is not successful as virus is constantly mutating
45
state what is meant by antibiotics
medicines that stop bacterial infections by killing them or inhibiting their reproduction
46
compare between bactericidal and bacteriostatic antibiotics
-bactericidal antibiotics kill bacteria by damaging bacterial cell wall so bacterial cells fail at undergoing osmotic control leading to lysis and death -bacteriostatic antibiotics inhibit bacterial growth by blocking enzymes needed for replication and protein synthesis
47
explain how antiviral drugs function
-they block viral receptors on surfaces of host cells -so viral particles cant bind or inject its core into the host cell which prevents lysis of host cells -some antiviral drugs work by blocking enzymes responsible for viral replication
48