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ODDR- Immunology > Immuno-pathology and HIV (E-lec) > Flashcards

Immuno-pathology and HIV (E-lec) Flashcards

1
Q

Define hypersensitivity reactions

A

An abnormal or exaggerated reaction to the ingestion, inhalation, or contact with a substance that does not provoke such a reaction in most people.

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2
Q

What is the apatite immune system sometimes triggered by?

A

triggered by non-self antigens that do not originate from an infectious agent

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3
Q

What are allergies provoked by antigens called?

A

allergens

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4
Q

What are the different classification of hypersensitivity reaction?

A

Types I, II, III and IV.

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5
Q

What are the different types of hypersensitivity reactions grouped according to?

A

Reactions are grouped according to the immune effector mechanisms that mediate the response and type of antigen that stimulates them

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6
Q

What is Type I Hypersensitivity caused by?

A

IgE binding to common, harmless allergens mainly air-borne allergens such as pollen and dust mites

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7
Q

What is a common source of allergen for Type I hypersensitivity reactions?

A

inhalation

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8
Q

Go through the process of sensitisation

A
  1. Soluble allergen is released from inhaled particles when they land on the mucosal surfaces
  2. allergen diffuses and can be picked up by dendritic cells
  3. Provokes an immune response that generates IgE producing plasma cells which migrate back to the mucosa
  4. IgE that is secreted binds to mast cells via the IgE Fc region and the Fc receptors on the mast cell surface.
  5. The antigen/ allergen specific Fab fragment is still free to bind to the allergen should it be present.
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9
Q

What would happen if an individual was reexposed to a type I hypersensitivity allergen

A

The allergen may bind to the IgE molecules, which will trigger the Mast cell via signals through the Fc receptors, to degranulate.
This causes release of histamine which has the troublesome effects that we associate with asthma or rhinitis

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10
Q

What are histamines?

A

A potent inflammatory mediator which has the troublesome effects that we associate with asthma or rhinitis

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11
Q

At what speed do type 1 hypersensitivity reactions occur at?

A

Type I hypersensitivity reactions have a very rapid onset which can be evident seconds or minutes after exposure

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12
Q

What is the rapid response of a type 1 hypersensitivity reaction due to?

A

This rapid response is due to IgE mediated mast cell degranulation causing increased permeability of blood vessels resulting in redness (erythema) and swelling (oedema) if the response is to exposure in the skin.

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13
Q

What reaction would you get if you get a type I hypersensitivity exposure to the airways?

A

airway the mast cell activation will instead cause oedema and constriction of the smooth muscle, both will narrow the airway, which is what happens in allergic asthma.

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14
Q

What is Type I hypersensitivity is characterised by?

A

an immediate followed by a delayed response. Classic symptoms of inflammation can be seen, including erythema (reddening of the skin) and oedema (swelling).

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15
Q

What is Type II Hypersensitivity mediated by?

A 
Type II Hypersensitivity reactions are mediated by IgG class antibodies. 
The IgG antibodies bind to the small molecules when they are bound to the surface of cells or bound to an matrix.

can also be mediated by IgG antibodies that recognise cell surface receptors

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16
Q

What is Type II Hypersensitivity caused by?

A

caused by the effects of small molecules (themselves otherwise harmless) which binds to cell surfaces and so modify their structure.

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17
Q

What can type II hypersensitivity reactions result in?

A

The binding will result in the activation of effector functions via the interaction of IgG Fc regions and Fc receptors
This includes the activation of: phagocytosis of the labelled cells/ matrix particles, activation of complement and NK cells.

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18
Q

What can Type II hypersensitivity reactions sometimes be caused by?

A

This type of reaction can be caused by some drugs including antibiotics.
Antibiotics such as penicillin and cephalosporin are examples of drugs that can trigger type II hypersensitivity reactions.

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19
Q

How can antibiotics result in Type II hypersensitivity reactions?

A

Once bound to red blood cells or platelets, recognition by the drug specific IgG will ultimatly result in destruction of those cells which can result in anaemia or abnormal bleeding respectively.

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20
Q

What happens when an IgG antibodies recognises cell surface receptors ?

A

These antibodies will then bind to this receptor which is attached to the plasma membrane of a cell.
This binding of the receptor may cause it to switch on uncontrolled signalling.
Alternatively it may block any signalling through that receptor due to the antibody blocking the ability of the receptor to interact with it’s intended ligand.

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21
Q

Why does the binding and recognition of IgG antibodies to cell surface receptors elicit uncontrolled signalling?

A

The pathology of the reaction is due to the fact that the bound IgG interferes with the signalling capability of that receptor.

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22
Q

What does type III hypersensitivity reaction occur in response to?

A

Type III hypersensitivity reactions occur in response to soluble antigens

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23
Q

What is Type III Hypersensitivity mediated by?

A

Mediated by IgG produced in response to soluble antigen.

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24
Q

What happens between the antigen and the IgG antibody?

A

. These antibodies and the antigen cluster together to form aggregates, called immune complexes. These complexes can trigger immune effector functions and cells, causing tissue damage and pathology.

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25
Q

What is the extent and type of damage determined by in a Type III hypersensitivity reaction?

A

determined by the size of the immune complexes and the amount of them present.
Larger complexes are more readily cleared by phagocytosis but smaller complexes may be deposited on blood vessel walls where they attract and activate complement and leukocytes resulting in damage to the blood vessels and tissue.

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26
Q

Give a systemic example of a type III hypersensitivity reaction?

A

Serum sickness

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27
Q

What is the treatment for Serum sickness?

A

It follows injection with a treatment containing lots of foreign protein, such as an anti-venom made from animal serum or a blood product.
An IgG antibody response against these injected proteins is produced

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28
Q

When do the symptoms for type III hypersensitivity reactions show?

A

after approximately 7-10 days post exposure to the antigen,

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29
Q

What does the time taken for symptoms of type III hypersensitivity reactions to show correspond with?

A

Corresponds to the amount of time it takes to raise an adaptive humoral (B cell) response where the B cells have also undergone class switching to produce antibodies of the IgG class.

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30
Q

What is type IV hypersensitivity reaction also known as?

A

Delayed type hypersensitivity reactions

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31
Q

What are type IV hypersensitivity reaction mediated by?

A

Mediated by antigen-specific effector T cells and not by antibodies

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32
Q

Which T cell types are involved in type IV hypersensitivity reactions?

A

The T cell types involved can be CD8 cytotoxic T cells or CD4 Th1 or Th2 helper T cells, which will deploy their antigen specific functions as if they were responding to a pathogen

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33
Q

What types of antigens/ allergens that cause type IV hypersensitivity responses

A

Typically the antigens/ allergens that cause these responses are small and can easily penetrate epithelial barriers such as the skin

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34
Q

What will the foreign molecules bind to in a type IV hypersensitivity reaction?

A

The foreign molecule will bind to host proteins, altering their structure and making them “look” different in an immunological sense, so they will now be seen as foreign and non self by the immune system.

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35
Q

What are the 2 responses to a type IV hypersensitivity reaction?

A
  1. Sensitisation

2. Elicitation

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36
Q

Describe the sensitisation response to a type IV hypersensitivity reaction?

A
  1. Initially the individual must first be “sensitized” to the allergen.
  2. Following the penetration of skin for example, dendritic cells take up the altered host proteins process and present it to T cells within a lymph node
  3. A T cell response is initiated and ultimately memory T cells are produced which will reside throughout the body.
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37
Q

Describe the Elicitation response to a type IV hypersensitivity reaction?

A

If an individual is exposed again to the same allergen the local antigen presenting cells will present it to the allergen specific memory T cells that reside there.

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38
Q

What is the pathology Type IV hypersensitivity caused by

A

can be caused by the the activation of Th1, Th2 or cytotoxic T memory cells.

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39
Q

What is an autoimmune disease?

A

A disease in which the pathology is caused by an adaptive response to self antigens or those present on our commensal microbiota.

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40
Q

When can autoimmune diseases occur?

A

Autoimmune disease can occur when the tissue damage cause by the auto-immune response exceeds the capacity for tissue repair.

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41
Q

What can autoimmunity be classified as?

A
  1. Organ-specific or

2. Systemic disease

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42
Q

Why does autoimmunity develop?

A

Autoimmune disease develops due to a combination of factors including,:
genetic susceptibility,
a breakdown in self-tolerance,
an environmental trigger such as infection.

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43
Q

What do most genetic defects causing autoimmune disease affect?

A
  1. defects that alter the amounts of cytokines and chemokines produced,
  2. defects in antigen presentation and defects that affect the lifespan
  3. proliferation of immune cells
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44
Q

How can infection trigger autoimmunity?

A

it may damage a cell or tissue barrier, releasing previously sequestered self antigens rendering them accessible to self reactive lymphocytes that may exist.

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45
Q

How can a pathogen cause an autoimmune disease?

A

A pathogen may produce a molecule that resembles a host protein and once the immune system has raised an immune response to the pathogen the effector cells and antibodies produced may then recognise and attack the similar host structure. This phenomenon is call “molecular mimicry”.

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46
Q

What is an organ specific immune disease?

A

The autoimmune diseases in which the pathology is restricted to specific organs can be called “organ specific”

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47
Q

What is a systemic specific immune disease?

A

The autoimmune diseases that involve pathology at many sites throughout the body can be defined as systemic autoimmune diseases.

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48
Q

Why is the effect of organ specific immune disease localised??

A

The autoantigens which the immune response is targeting are only expressed in one or a few organs and therefore tissue damage will be limited to those locations.

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49
Q

Give an example is an organ specific immune disease?

A

Type 1 Diabetes

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50
Q

What causes type 1 diabetes?

A

Caused by an immune response that attacks insulin producing β (beta) cells in the pancreas.

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51
Q

What is the major autoantigen for type 1 diabetes?

A

Insulin

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52
Q

Why is the effect of systemic autoimmune diseases more spread out?

A

As Tissue damage can occur a many sites spread throughout the body, wherever the autoantigen is present.

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53
Q

Give an example is a systemic immune disease?

A

Scleroderma

Rheumatoid arthritis

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54
Q

What is Scleroderma characterised by?

A

It is characterised by autoantibodies that are produced against ubiquitous autoantigens such as chromatin and components of mRNA processing machinery, which will be present in every cell.

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55
Q

What do some of the important mechanisms that lead to autoimmune diseases depend on>

A

2 involve autoantibodies, while a third is mediated by autoantigen specific T cells.

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56
Q

Describe the 1st mechanism by which the pathology of autoimmunity develops
(hint similar to the pathway underlying type II hypersensitivity reactions)

A

IgG or IgM autoantibodies recognise autoantigen on the surfaces of cells or the surfaces of extracellular matrix.

57
Q

Give an example of the 1st mechanism by which the pathology of autoimmunity develops and how it works

A

An example is acute rheumatic fever where antibodies raised against an antigen from Streptococcal species will then also binds to cardiac muscle the Fc regions of these antibodies will then recruit immune effector functions.

58
Q

Describe the 2nd mechanism by which the pathology of autoimmunity develops
(hint similar to the pathway underlying type III hypersensitivity reactions)

A

These reactions are mediated by IgG autoantibodies that recognise and bind to soluble autoantigens. These form immune complexes and the deposition of these complexes can trigger tissue damage where they are deposited.

59
Q

What is the 2nd mechanism by which the pathology of autoimmunity develops important for?

A

the pathogenesis of rheumatoid arthritis.

60
Q

Describe the 3rd mechanism by which the pathology of autoimmunity develops
(hint similar to the pathway underlying type IV hypersensitivity reactions)

A

It is mediated by autoantigen specific effector T cells. Both autoantigen specific cytotoxic T cells and T helper cells can be directly involved in mediating autoimmunity

61
Q

When was the first case of AIDs reported?

A

June 1981

62
Q

What did the Centres for Disease Control first describe HIV as in 1981?

A

They described it as a rare lung infection

63
Q

What does AIDS stand for?

A

Acquired immune deficiency syndrome

64
Q

When was the term Acquired immune deficiency syndrome first used?

A

1982

65
Q

What test was first carried out in 1985?

A

First test for antibodies is commercially available based on ELISA.

66
Q

Approx how many people are living with HIV?

A

35 million

67
Q

Why was the number of cases of people with HIV increasing between 2001 and 2005?

A

HIV transmission is continuing but the numbers of people dying from AIDS related causes has been reduced by the expanded availability of anti-retroviral drugs. Although the rate of new infections globally has slowed the reduced death rate has lead to an increase in the numbers who are currently living with HIV infection.

68
Q

Which country has the highest number of people affected with HIV?

A

Sub-saharan Africa

69
Q

Approx hope many deaths are caused by AIDs globally?

A

1.5 million

70
Q

What percentage of people living with HIV are thought to be unaware of their infection?

A

54%

71
Q

What is the reason for the lower mortality for AIDs now?

A

due to the wider availability of HIV related drugs and slower transmission rate.

72
Q

Name the 2 major types of HIV that have been identified?

A

HIV-1 and HIV-2

73
Q

How did HIV-1 and HIV-2 spread to humans?

A

from different animal reservoirs

74
Q

Which primate was the reservoir for HIV 1 transmission

A

Chimpanzee

75
Q

Which primate was the reservoir for HIV 2transmission

A

sooty mangabey

76
Q

Which virus are both HIV-1 and HIV-2 related to?

A

primate Simian Immunodeficiency Viruses, (SIV).

77
Q

What is HIV further split into?

A

3 groups:
Group M
Group N
Group O

78
Q

Which of the 2 types of HIV is responsive fo the majority of AIDs cases world wide?

A

HIV 1

79
Q

Where is HIV 2 more prevalent?

A

It is an endemic in West Africa and is spreading in India.

80
Q

Describe the structure of HIV 1

A
  1. 2 copies of single stranded RNA genome.
  2. Virus surface protein gp120 via which HIV infects host cells that express CD4
  3. Numerous copies of viral enzymes required for initial infection stages.
81
Q

How does HIV 1 gain entry into the host cell?

A

via proteins on the surface of the virion (gp120 and gp41). gp120 binds with high affinity to CD4 and a chemokine co-receptor.

82
Q

HIV can only effect cells with which repceptor?

A

receptor CD4, this is called it’s cellular trophism

83
Q

Which cells express the CD4 receptor (cellular trophism)?

A

T helper cells express CD4 and are therefore infected by HIV.

84
Q

What type of virus is HIV?

A

A retrovirus

85
Q

How does the HIV genome encode for many proteins when it is very short?

A

The HIV genome is very short but encodes many proteins because:

  1. the genome can be read in 3 different reading frames
  2. long polypeptides cleaved to release multiple functional proteins.
86
Q

What does the gp41 protein do?

A

The gp41 virus protein causes the membranes of the virus particle and the host cell to fuse after the virus has entered the host cell
This fusion helps deliver the nucleocapsid and it’s contents (viral genome and essential enzymes) into the host cell.

87
Q

What are the virions enclosed in?

A

The virions are enclosed by a membrane envelope and also contain 2 other structural proteins gp17 and gp24 (the nucleocapsid protein).

88
Q

When and How do the viruses gain their membrane envelope?

A

They gain it when they bud off from an infected cells plasma membrane and are released

89
Q

What do HIV virons do when they inject a cell?

A

Viruses hijack host cell machinery, using it to replicate and produce more virions
But HIV has essential enzymes that provide functions that cannot be performed by any host protein.

90
Q

What dies the HIV reverse transcriptase enzyme (p64)

A

This enzyme is required to transcribe the viral RNA genome strands into a complementary DNA (cDNA) strands

91
Q

Why is the HIV reverse transcriptase enzyme important?

A

Because proteins of the host cells (human proteins) can only perform transcription in the direction of DNA to RNA.
So reverse transcriptase changes the viral RNA into cDNA

92
Q

What happens to the cDNA following reverse transcription?

A

the cDNA encoding the viral genes enters the nucleus along with the protein integrase (p32) and is integrated into the host DNA genome by this integrase enzyme.

93
Q

What does the integration of cDNA into the host DNA genome allow?

A

The viral genes can now be transcribed by the host into mRNA sequences from which viral proteins are translated, and new virions can be produced.

94
Q

What is the HIV protease enzyme required to do?

A

It is required to cleave some long polypeptide chains translated from viral mRNAs releasing multiple individual functional proteins.

95
Q

Summarise the stages involved in HIV viral replication

A
  1. HIV enters cell via viral gp120 binding to host CD4, and fusion via gp41
  2. Reverse transcription of viral RNA genome to cDNA by viral reverse transcriptase
  3. Integration of viral cDNA into host genome by viral integrase
  4. Viral genes transcribed and translated by host
  5. Multiple virus particles assembled and bud from the cell, acquiring membrane envelope.
96
Q

How does hIV infection kill CD4 positive cells?

A

By 3 mechanisms:

  1. Virus Cytopathicity.
  2. Apoptosis.
  3. Cytotoxic T cells.
97
Q

Describe how the HIV virus can kill CD4 positive via the virus Cytopathicity mechanism

A

Direct killing,
cell integrity lost,
overwhelmed by virus production

98
Q

Describe how the HIV virus can kill CD4 positive via the Apoptosis mechanism?

A

Infected cells are more likely to undergo apoptosis

99
Q

Describe how the HIV virus can kill CD4 positive via the Apoptosis mechanism?

A

HIV specific T cells will recognise and kill infected CD4 positive cells.

100
Q

What foes an acute infection caused by a virus induce?

A

induces an immune adaptive response that eliminates the infection and results in lasting protection, through immunological memory

101
Q

How I lasting protection achieved following a viral infection?

A

Through immunological memory and the production o memory cells

102
Q

What type of infection do herpes like viruses set up?

A

“latent” infection

103
Q

What is a laten infection?

A

It is an infection that isn’t eliminated but is chronic and controlled by the adaptive response

104
Q

What does untreated HIV infection lead to?

A

Untreated HIV infection reduces CD4 T cell numbers, subsequent immune deficiency leads to death due to opportunistic infections or cancer

105
Q

When does the acute phase occur in a HIV infection?

A

The acute phase occurs in the first weeks post infection

106
Q

What is the acute phase of a HIV infection characterised by?

A

characterised by flu-like symptoms in 80% of cases.

107
Q

Describe the blood composition during the acute phase of a HIV infection

A
  1. Abundance of virus particles in the patients blood
  2. adaptive immune response produces antibodies
  3. cytotoxic CD8 positive cytotoxic T cells that are specific for HIV derived antigens
108
Q

What do cytotoxic T cells do?

A

cytotoxic T cells will recognise and kill infected cells.

109
Q

What is the appearance of antibodies in the blood known as?

A

seroconversion

110
Q

What happens to the number of CD4 T cells during infection?

A

Initially there’s is a dramatic decrease in CD4 T cells

Following the initial immune response CD4 T cell numbers then partially recover

111
Q

What follows the acute phase?

A

asymptomatic phase

112
Q

What does the virus do during the asymptomatic phase?

A

and continues to replicate and CD4 T helper cell numbers gradually decline

113
Q

How long can the asymptomatic phase last?

A

anywhere between 6 months and 20 years

114
Q

What does the asymptomatic phase end with?

A

ends when CD4 T cells have fallen to approximatley 500 per microlitre of blood.

115
Q

At what level is there an are insufficient number of CD4 cells to provide immune protection ?

A

Less than 500 per microlitre of blood

116
Q

What happens when the number of CD4 cells falls below 500 per microlitre of blood?

A

There is no longer a sufficient number of CD4 cells to provide immune protection and opportunistic infections become increasingly frequent during this symptomatic phase.

117
Q

How low does the CD4 T cell number need to be for the disease to be considered AIDs?

A

When the CD4 T cell number drops below 200 cells per micro litre the patient is said to have AIDS

118
Q

What do antiretroviral drugs do?

A

They suppress HIV replication fora patients lifetime

119
Q

Describe the change in the number of infectious virus particles in the blood plasma when a patient is infected with HIV

A

4-8 weeks in virus particles increase dramatically
Then dramatic decrease due to death of infected CD4 T cells
They fluctuations in the number of virus particles but gradual increase generally

120
Q

Describe the change in the number of antibodies in the blood plasma when a patient is infected with HIV

A

Increase for first 4-8 weeks
Then levels off
Then decreases after 15 wish years as immune response is compromised

121
Q

What happens once the CD4 levels drop below critical levels?

A

The immune system collapses and the individual is said to have AIDS.

122
Q

What can people with AIDs die from?

A

A variety of opportunistic infections can kill people with AIDS.

123
Q

Where are opportunistic pathogens present?

A

Opportunistic pathogens are present in the normal environment but will only cause severe disease in the immunocompromised.

124
Q

How does HIV escape elimination by the immune response to always result in AIDS in the absence of treatment?

A
  1. CD4 T cells are required to assist in controlling the infection. HIV’s trophism means T cells are destroyed.
  2. The antibodies produced in an immune response do not bind well to intact virus particles of infected cells.
  3. HIV rapidly mutates, new mutant forms may escape recognition by neutralising antibodies or clones of specific CD8 T cells that have expanded to eliminate the infection.
125
Q

How do mutant variants of HIV appear rapidly?

A

due to it’s fast rate of replication and high mutation rate during replication.

126
Q

Why is there a high mutation rate when HIV is dividing?

A

The mechanism of reverse transcription is error prone because the reverse transcription enzyme lacks the proofreading systems of the host DNA polymerases.
Therefore mistakes in the sequences of cDNA to be integrated into the hosts DNA occur and will result in mutant viral proteins being produced.
Further mutations are produced when RNA polymerase II transcribes the integrated viral DNA into RNA sequences

127
Q

What causes HIV drug resistance occur?

A

The rapid accumulation of mutations in the HIV genome leads to drug-resistance in addition to escape from immune responses.
HIV can become resistant to any of the known anti-HIV drugs. Resistant variants emerge rapidly following treatment with individual drugs.

128
Q

When is anti HIV treatment successful?

A

Anti-HIV treatment is only successful if drugs are taken in combination

129
Q

What does the the rapid accumulation of mutations within the viral genome lead to?

A

affords HIV the ability to rapidly develop resistance to drugs

130
Q

What does drug treatment initially do ?

A

Drug treatment will initially dramatically reduce viral particle production, but any resistant variants present will be able to replicate and will emerge and multiply until previous virus levels are soon reached again.

131
Q

What does Post exposure prohylaxis PEP involve?

A

administering of a combination of standard anti-HIV drugs shortly after suspected exposure to HIV.

132
Q

What does Post exposure prohylaxis PEP prevent?

A

PEP may prevent HIV establishing infection if administered up to 72 hrs post exposure.

133
Q

What has most anti HIV drug development focused on?

A

Most of the drug development efforts have been focussed on targetting the few essential viral proteins that must be taken into the host cell at the time of infection, those that cannot be found in an uninfected host, such as the HIV reverse transcriptase enzyme and the viral protease

134
Q

What drug families are involved in Post Exposure Prophylaxis. ?

A
  1. Nucleoside/ nucleotide reverse transcriptase inhibitors.
  2. Non-nucleoside reverse transcriptase inhibitors.
  3. Viral protease inhibitors.
  4. Fusion and entry inhibitors.
135
Q

Where is the lily source of HIV in saliva?

A

In GCF

136
Q

Is HIV transmissible by saliva.

A

Saliva usually contains non-infections HIV components thus HIV is rarely transmissible by saliva.

137
Q

What form ofAnti- HIV factors does saliva contain

A

Saliva contains anti-HIV factors that block the infectivity of the virus.

138
Q

What are some anti HIV factors found In saliva?

A
  1. Salivary mucins may clump virus particles together
  2. Salivary mucins and agglutinin may strip HIV of gp120
  3. Secretory Leukocyte Protease Inhibitor (SLPI) produced by salivary glands binds to T helper cells and blocks HIV-1 gaining access and infecting the cells.

ODDR- Immunology (6 decks)

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