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Medsci 314 > Lecture 22; Immunity to infection part two > Flashcards

Lecture 22; Immunity to infection part two Flashcards

1
Q

Write some notes on parasite + worm infections;

A
  • most parasites are host specific (receptor specificity)
  • many parasites have complicated life cycles, often involving more than one host (e.g. insects, snails, human)
  • many parasite infections are chronic
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2
Q

Write some notes on parasite antigens;

A
  • certain antigens are only expressed at certain stage of development
  • greater variety and quantity of antigens compared to bacteria
  • antigenic variation is common
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3
Q

Give an example of parasite antigenic re-arrangemnt and what causes this;

A

Programmed DNA rearrangement
e.g. Trypanosoma ssp (insect-borne protozoa)
VSG: variant specific glycoprotein

They are eukaryotic so many antigens

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4
Q

Whats a parasite transmitted by the sand fly?

A

Leishmaniasis (aka Orient Boil, Kala-azar, Black fever, Sandfly disease, Dum-Dum fever, Baghdad Boil)

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5
Q

Write some overview notes on leishmaniasis;

A
  • transmitted by sandfly
  • causes damage to spleen and liver
  • intracellular protozoa (macrophages)
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6
Q

What is the nature of response to leishmaniasis?

A

Th1 or TH2

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7
Q

Describe Th1 response to leishmaniasis;

A

Baghdad boil (cutaneous leishmaniasis)

Th1 response:

  • vigorous host cellular response
  • many immune cells in lesions
  • limited disease
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8
Q

Describe Th2 response to Leishmaniasis;

A

Kala-azar (visceral leishmaniasis)

Th2 response:

  • defect in cell-mediated immunity
  • humoral response (useless as IC)
  • adequate antibody response, but ab cannot reach intracellular parasite
  • many parasites in lesions (highly infectious form of disease)
  • disseminated disease
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9
Q

Whats transmitted by the anopheles fly?

A

Malaria

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10
Q

Write some short notes about malaria;

A

Plasmodium falciparum (80% of malaria infections and 90% of malaria deaths) Plasmodium vivax, P. malaria, P. ovale
- transmitted by Anopheles fly
- natural protection against malaria:
“sickle-cell” disease (mutation in Hb gene)

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11
Q

Describe the life cycle of plasmodium;

A

Two life cycles

  • one in the fly
  • One in humans

Each step develops into different forms.

In RBC and Liver hepatocytes. Each time the immune system must learn to recognise it again

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12
Q

Describe the plasmodium stage of development and T cell response;

A

Sporozites in blood = Th2 (Ab production)
Tissue Shizonts in liver = Th1 (pro inflam)
Merozites in blood = Th2 (Ab production)
Aseuxal erythrocyte stage = TH1/Th2 (Ab and Pro-inflam)

Point being that each stage is different antigen therefore different response. Hard to cure as some moves on to the next stage so previous AB no effective without meds

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13
Q

What is blood flukes?

A

Schistosoma

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14
Q

What are some examples of Schistosoma?

A

Schistosoma mansoni

Schistosoma haematobium (bladder fluke)

Lots of intermediate stages therefore require several hosts

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15
Q

Write some notes on; Schistosoma mansoni

A

Schistosoma mansoni
- larvae are released from water snail and penetrate skin
migration through blood and lung to hepatic portal vein

= (adult worm) Intestinal Schistosomiasis / Snail Fever

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16
Q

Write some notes on; Schistosoma haematobium (bladder fluke)

A 
Schistosoma haematobium (bladder fluke)
- larvae are released from water snail and penetrate skin migrate to veins of bladder

= Urinary Schistosomiasis

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17
Q

Whats a challenge with an immune response to schistosome larvae?

A

Theyre very large so cant just be phagocytosed

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18
Q

Whats a key cell in the schistosome larvae response?

A

mast cells; They recognise parasite specific antigens then become activated releasing histamine and heparin which are toxic to the parasite.

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19
Q

What is the typical response for worm infections?

A

Th2 (Dominant)

  • Characterised by anti-inflam cytokines such as IL4, 5
  • Stimulation and maturation of B cells, which critically produce antibodies.
  • Compliment activation
  • Then get a number of cells i.e macros, neutros, eosinophils that bind to the Fc region of Ab and release toxic substances.
  • AB is critical for this process.
  • Some Th1 + proinflam for macro activation

= ADCC

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20
Q

Write some general notes on viruses;

A
  • obligate intracellular parasites (depend on host metabolism to survive)
  • high structural and genetic diversity (high mutation rate)
  • host specific (infection depends on specific receptors on host cell)
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21
Q

Write some notes on the general innate immune response to viruses;

A
  • IFN stimulates inhibition of viral replication
  • NK cells are cytotoxic for virally infected cells
  • complement can damage virion envelope (virolysis)
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22
Q

Write some notes on the general adaptive immune response to viruses;

A
  • antibodies limit viral spread and re-infection

* cytotoxic CD8 T cells: destroy virus-infected cells

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23
Q

Whats the role of cytokines when a cell becomes infected?

A

The infected cell releases type one interferon i.e IFNa,b

These induce the production of

  • PKR: protein kinase R phosphorylates eukaryotic translation initiation factor 2 (eIF2) (this stops protein production)
  • Ribonucleases: cleave RNA

Which creates defence in the neighbouring cell

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24
Q

What cells do the type one interferons recruit?

A

NK cells (innate)

  • Kill cells with low MHC 1
  • ADCC
  • Releases type 2 (IFNg) interferon
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25
Q

What is the role of IFNg (type 2) in the immune response?

A

It boosts the production of the proteins in cells (PKR, RIbonucleases) to protect from viruses and recruits TH1

TH1
= Adaptive response

26
Q

What role to antibodies play in preventing virus infection?

A

Virus’ typically invade through the mucosal sites.

IgA and IgG neutralise them and prevent their spread.

27
Q

What role does AB play with infected cells?

A

IgM IgG bind to the infected cell.

Ab mediated compliment activation.

or

opsonisation via Fcγ and complement receptors on macrophages

or

ADCC

28
Q

Whats a particular target of virus immune evasion?

A

endogenous MHC type one pathway

They interfere with different stages.

29
Q

Describe the different stages MHC type one can have interfered with my viruses.

A

MHC 1 downregulation

MHC 1 retrotransport (not expressing it on surface)

MHC 1 retention (not expressing on surface)

ER associated protein degradation

30
Q

What is immunodeficiency disease?

A

Immunodeficiency disease: results from absence or failure of normal function of one or more elements of the immune system

I.e AIDS

31
Q

How can immunodeficiency disease be categorised based on specificity?

A

Specific immunodeficiency: involves B and T cells (adaptive immune system), e.g. severe combined immunodeficiency (SCID), adenosine deaminase (ADA) deficiency

Non-specific immunodeficiency: involves complement, phagocytes (innate immune system.)

32
Q

How can immunodeficiency be further classified based on origin?

A

Primary immunodeficiency: due to intrinsic defects, mostly genetically determined SCID, ADA (adenosine deaminase) deficiency

Secondary immunodeficiency: acquired defects (drugs, malnutrition, HIV)

33
Q

What are the two types of HIV?

A

• Two major types: HIV1 (more virulent) and HIV2 (endemic in West Africa)

34
Q

What are the host cells for HIV?

A

• Host cells: CD4 T cells, dendritic cells, macrophages.

35
Q

How can HIV be transmitted?

A
  • sexual intercourse
  • contaminated needles (illicit drug user)
  • use of infected blood or blood products
  • breast feeding by infected mother
36
Q

What does cellular tropism mean and how does it apply to HIV?

A

ability to enter particular cell type based on expression of specific host cell receptors.

Can enter two different cell types

  • Lymphocyte-tropic virus “X4 viruses”
  • Macrophage-tropic virus: “R5 viruses”
37
Q

Write some notes on Lymphocyte-tropic virus “X4 viruses”

A

Lymphocyte-tropic virus: uses CXCR4 (chemokine receptor_, needs high levels of CD4 “X4 viruses” on T cells

38
Q

Write some notes on Macrophage-tropic virus: “R5 viruses”

A

Macrophage-tropic virus: uses CCR5(chemokine) as co-receptor and requires “R5 viruses” only low levels of CD4
CCR5 is expressed on DC, Macrophage activated T cells

39
Q

Describe the life cycle of HIV;

A

Binds to host cell CD4 and co receptor

Get taken up by cell and release their genetic material (RNA) and they carry reverse transcriptase. Turns RNA into DNA

DNA travels into nucleus and integrates into genome when chromosomes replicate.

Once in a while it is transcribed and HIV RNA is formed and this forms the virus and can leave the cell.

40
Q

Describe the initial time course of an untreated HIV infection

A
  • primary (acute) infection is often asymptomatic or causes Flu-like (or mono- nucleosis-like illness.) Due to sudden drop in CD4 numbers!!!
  • HIV first infects DC, which ‘carry’ the virus to the lymph node. (vigorous HIV replication due to many T cells)
  • lack of protective immune response results in viremia
  • drop in circulating CD4 T cells due to activation of CD8 T cells
41
Q

Describe the immune response of untreated HIV after the initial infection

A
  • CD4 T cell number rebounds (asymptomatic period or clinical latency)
  • production of antibodies (sero-conversion). Important for diagnostic. Virus replicating in lymphoid tissue. Patient feels well.
  • gradual decline of CD4 T cells (symptomatic phase). Development of lymphadenopathy (swelling of lymph nodes), fever, sweating, weight loss. AIDS
42
Q

How does HIV escape the immune system in terms of genetic variation?

A
  • High replication and mutation rates (quasi species develop into escape variants).
  • Antigenic variation: immunogenic surface proteins (gp41 and gp120) develop new epitopes not recognised by CTLs.
  • HIV interferes with synthesis of MHC class I proteins.
43
Q

Describe how HIV escapes the immune response in a non-genetic way;

A
  • Neutralising antibodies: control HIV particles in blood, but can’t eliminate virus altogether
  • Provirus “hides” inside the cell on host chromosome (latent infection).
44
Q

What are the potential noteable points for HIV therapies;

A
  • Protease inhibitors
  • CCR5 inhibitors
  • CXCR4 inhibitors
  • Reverse transcriptase inhibition
45
Q

Whats an example of an HIV treatment that stops RNA replication due to lack of an OH group?

A

• nucleoside analogues RT inhibitor (NRTI), e.g. Azido-thymidine (AZT, Zidovudine, Retrovir)

46
Q

Whats another HIV treatment example?

A

• HAART: highly active antiretroviral therapy, protease inhibitor combined with 2 or more RT inhibitors

Several combined drugs

47
Q

Write some notes on important influenza virus structures;

A

Genome: 8 single-stranded, negative sense RNA segments

hemagluttinin (HA)
Neuraminidase (NA)

48
Q

What is hemagglutinin?

A

Hemagglutinin (HA): binds to sialic acid-containing receptors on epithelial cells of host.

49
Q

What is neuraminidase?

A

Neuraminidase (NA): cleaves sialic acid at the end of virus life cycle to allow mature
virions to be released.

50
Q

What is the innate response to influenza?

A

• Type I interferons provide virus resistance
Viral replication/cell lysis leads to production of IL-1, IL-6, IL-8, TNF, IFN-γ (inflammatory response). Disease symptoms (fever, cough, etc).

51
Q

What is the adaptive immune response to influenza?

A
  • Viral clearance correlates with appearance of HA and NA specific CD8 T cells in lung
  • efficient clearance and protective immunity requires CD4 T cells (production of primarily IgG and IgA (neutralisation of HA - subtype specific)
52
Q

What are the two types of antigenic variation that can exist in influenza?

A

Antigenic Drift

Antigenic Shift

53
Q

What is antigenic drift?

A

Typically genomic variation

But if HA or NA are altered then new escape variant is formed.

54
Q

What are the NA and HA sub types associated with humans?

A
  • 16 non-overlapping subtypes of HA, but only 3 are associated with human disease (H1, H2, H3).
  • 9 non-overlapping subtypes of NA, but only 2 are associated with human disease (N1, N2)
55
Q

Describe influenza receptor specificity;

A

Human HA types: bind 2-6 sialic acid receptors
Avian HA types: bind 2-3 sialic acid receptors

Pig HA types: bind both receptor

56
Q

What is antigenic shift;

A

If two seperate strains of influenza (one human one bird one) meet i.e in pig, and they exchange RNA then a new strain can be formed that can infect humans

Number of AA changed

57
Q

When do pandemics normally evolve?

A

Following antigenic shift

58
Q

What are the two therapies for influenza?

A

NA inhibitors:

Adamantane derivatives:

59
Q

Write noes on NA inhibitors;

A

NA inhibitors: oseltamivir (Tamiflu), zanamivir

  • inhibit viral replication , reduce NA activity
  • use of oseltamivir against bird flu H5N1 in Vietnam and Thailand failed !
60
Q

Write notes on adamantane derivitives;

A

Adamantane derivatives: amantadin, rimantadine - decrease viral shedding
- rapid development of resistant viruses

61
Q

What about influenza vaccines?

A
  • “Flu-shot”: inactivated virus
  • Nasal spray flu vaccine: attenuated virus (LAIV = live attenuated influenza
    vaccine)
    Both vaccines contain H1N1 and H3N2 strains
    Vaccine changes each year based on international surveillance of circulating influenza A viruses.

Medsci 314 (31 decks)

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