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Immunology and Infection > Antigenic Variation > Flashcards

Antigenic Variation Flashcards

1
Q

what is the antigen?

A
  • anything that an antibody will recognise

- antigens can vary, which can be evolutionary advantage

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2
Q

what are the two important proteins in influenza?

A

hemagglutinin (attaches to host receptors)

neuraminidase (breaks down sialic acid to allow budding)

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3
Q

what is antigenic drift?

A

minor mutations

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4
Q

what is antigenic shift?

A
  • major reassortment
  • virus infecting different species recombine leading to a major genomic change
  • leads to pandemics
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5
Q

what are the 3 subspecies of Trypanosoma brucei?

A
  1. T. brucei brucei
  2. T. brucei gamiense
  3. T brucei rhodesiense
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6
Q

what is T. brucei spread by?

A
  • the Tseste fly (infecting bile)

then you have haemo-lymphatic stage 1, meningo-encephalitic

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7
Q

what are the key points of how T. brucei achieves variation?

A

they switch surface coats - have variance surface glycoproteins (VSG surface coat)

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8
Q

what stages are VSG genes expressed by in T. brucei ?

A
  1. metacyclic

2. blood stream

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9
Q

how many VSG genes can the blood stream express?

A
  • around 1000 VSG genes
  • only one at a time
  • switch rate: every 100+ divisions
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10
Q

where does T. brucei survive?

A

the bloodstream - extracellular

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11
Q

how does the VSG in T.brucei work?

A
  • tight protection coat
  • not accessing other proteins expressed
  • comes in waves
  • waves from the slender form to the stumpy form
  • stumpy forms dont divide
  • variant A will decline
  • variant B is produced and increases
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12
Q

describe the process of VSG switching

A
  • entire VSG is internalised and recycled in 12.5min cycles
  • any antibody that lands on the antigen is digested
  • basis for evasion of the immune response
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13
Q

where is the VSG most variable?

A

Ab binding region

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14
Q

what type of genes are VSGs?

A
  • pseudogenes or gene fragments
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15
Q

how does T.brucei create new genes?

A

recombining fragments

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16
Q

where are expressed VSG genes located?

A
  • telomeric expression site (ES)

- only one expressed but multiple expression sites

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17
Q

how many expression genes are in the trypanosome nuclear genome?

A
  • around 20

- but only one is active at any given time

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18
Q

what does the telomere location of VSG expression sites suggest?

A

a role for position effect in their regulation

- specific structural features are associated with the DNA at ‘silent’ telomeres in blood stream trypanosomes

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19
Q

what are the mechanisms of activation for homologous recombination/gene conversion proposed in T.brucei?

A
  1. gene conversion
  2. segmental gene conversion
  3. telomere exchange
  4. transcriptional switch
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20
Q

what is gene conversion in t.brucei?

A

VSG expressed is swapped for another

21
Q

what is segmental gene conversion in t.brucei?

A
  • multiple recombination

- made of multiple gene fragments

22
Q

what is telomere exchange in t.brucei?

A

from another expression

23
Q

what is transcriptional switch?

A
  • one expression site shut down another switched on
24
Q

what is the structure of a VSG expression site?

A
  • 50bp repeats upstream of promoter
  • 70bp, instrumental in recombination
  • ESAGS
  • VSG promoter ~50kb of VSG gene
25
what are ESAGS in VSG?
- expression site associated genes | - driven by polymerase 1
26
what is the model for telomeric silencing in t.brucei?
- silencing involves separate telomere binding and spreading factors - remove Rab repressor - T.brucei will express all 3 VSG coats
27
how are enzymes used in the VSG of t.brucei?
- mutants of enzymatic pathway show de-repressed VSG transcription - polymerase I expression limited through a kinase
28
what causes antigenic variation in plasmodium?
Var genes
29
what does plasmodium cause?
malaria
30
why is plasmodium difficult to target for vaccines and treatments?
complex lifecycle
31
give a brief overview of the human lifecyle of plasmodium
- goes to the human liver first - merozoites then infect the RBCs - they are burst and destroyed - cause anemia and fever - produce gametes which are taken up by the mosquito
32
when are the cycles of fever and chills in malaria?
- every 48 hours - related to the bursting of RBC and the release of parasites - malaria is highly pathogenic
33
how does the plasmodium transform the RBC?
- has knobs and cytoadherence - infected RBCs develop suface knobs containing parasitic proteins - causes the RBC to stick in blood vessels and block capillaries (RBC not cleared) - forms clumps - results in liver and brain inflammation
34
what is the main protein involved in the cytoadherence caused by plasmodium?
PfEMP1 - promotes parasite survival | - these proteins are transcribed throughout the genome
35
what is PfEMP1 coded by in plasmodium?
Var genes
36
what are the highly variable domains in PfEMP1?
1. DBI domain | 2. CIDR domain
37
how do the DBI and CIDR domains cause variability in the plasmodium?
- recombine and theres different categories | - can recombine with themselves and with each other
38
where is PfEMP1 found?
on the surface of the host cell (rather than the parasite surface)
39
how has T.cruzi been targeted?
targeting the vector rather than the parasite
40
what strategy does t.cruzi use to evade the immune system?
the invisible cloak strategy
41
what does the invisible cloak strategy entail in t.cruzi?
- multiple copy families of surface antigens - lots of duplication - hard to classify because their surface proteins change - they can (theoretically) infect any nucleated cell
42
how does t.cruzi overwhelm the immune system?
50% of genome is surface proteins and they are all expressed
43
what are the main 3 highly heteregenous gene families in t.cruzi?
1. trans sialidases 2. mucins 3. MASPs
44
what are trans-sialidases in t.cruzi?
- catalyses the transfer of silaic acid - bind to host cell receptors to invade - block complement/immune evasion
45
what are mucins in t.cruzi?
- major acceptors of sialic acid | - form a thick surface barrier of different lifecycle stages
46
what are MASPs in t.cruzi?
- highly polymorphic gene family - enable t.cruzi to invade and multiply in the cytoplasm of host cells - implicated in infertility; also reduce virulence
47
how does t.cruzi fool the immune systeM/
fools T cells into thinking the parasites are self
48
what does t.cruzi need sialic acid for?
- host cell attachment - invasion of the cytosol - host mimicry
49
how does t.cruzi obstruct CD8+ T cell immunity?
- immune cell function dependent on sialic acid - activated when they lose sialic acid - puts them back on to the T cells to confuse the T cells - T cells are inactive and dont target the parasite

Immunology and Infection (13 decks)

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