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Immunology Infection And Inflammation > Infection And HIV > Flashcards

Infection And HIV Flashcards

1
Q

What is the host defence strategy for attachment?

A

Rinse away by surface host secretion (trachea-cilia) and IgA

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2
Q

What are the microbial strategies to overcome host attachment defences?

A

Microbes surface molecules attach to receptors on epithelial cells. Produce ciliatoxic molecules and IgA protease.

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3
Q

What is the host defence strategy for invasion?

A

Cell membrane is used as a barrier.

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4
Q

What are the microbial strategies to overcome host invasion defences?

A

Traverse the membrane of have phagocytise uptake. Fusion proteins in the viral envelope and release proteins that block intracellular killing.

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5
Q

How can a microbe defend against a phagocyte?)

A

Release leukocidins and antiphagocytic haemolysins. Which are cytotoxic to macrophages. And they use components of cell wall/ membrane to inhibit phagocytosis.

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6
Q

How do microbes counteracts host defence of restriction of Fe(3)?

A

The release siderophores, which bind and import iron into the cytosine where it’s released.

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7
Q

How do microbes counteract the production of anti microbial peptides?

A

Microbes alter the cell surface receptors and release processes to break them down.

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8
Q

What exit strategies do microbes have?

A

Stimulate host processes for transmission. Eg: sneezing, diarrhoea. Most processes that release bio fluids.

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9
Q

How does the cholera toxin enter the cell?

A

It binds to enterocyte GM1 receptor and is endocytosed to the ER.

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10
Q

What does the cholera toxin release from the ER?

A

A1 diffuses to Adenylate Cyclades to catalyse ribosylation of Gs Alpha subunit.

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11
Q

What happens when cholera toxin ribosylates G-alpha?

A

Increase GTPase activity, increased cAMP which cause eflux of ions and the water by osmosis leading to diarrhoea

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12
Q

What does the cholera toxin do?

A

Bind GM1 receptors, cause release of A1 from the ER this ribosylates cAMP increase GTPase activity. Leads to increased cAMP causing eflux of ions leading to osmosis and finally diarrhoea

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13
Q

What does Enterotoxigenic E.coli do?

A

Attaches small intestine mucosa and releases heat labile and stable toxins.

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14
Q

What does Enteropathogenic E.coli?

A

Attach firmly to intestinal mucosa and cause dissolution of the brush border by vesiculation of microvilli.

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15
Q

What does Enteroinvasive E.coli do?

A

Attach to colonic enterocytes and causes necrosis and strips areas of colonic mucosa.

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16
Q

What is necrosis?

A

Form of premature cell death (autolysis) can be caused by toxins

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17
Q

What is enteroaggregative E.coli?

A

Damage and blunt villi via haemorrhagic necrosis

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18
Q

What is enterohaemorragic E.coli?

A

It is an E.coli that releases shifts like toxins which kill enterocytes cause haemorrhagic colitis.

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19
Q

What haemorrhagic colitis?

A

Severe cramping and diarrhoea that becomes bloody

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20
Q

What are islands of pathogenicity?

A

Areas of pathogenic genes usually from horizontal gene transfer.

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21
Q

What is a major island of pathogenicity?

A

Locus of enterocyte effacement (LEE) which encodes for proteins that allow the injection of Enterohaemorhagic E.coli proteins into host cell.

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22
Q

How many types of shiga like toxin are there?

A

2

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23
Q

How does shiga like toxin work?

A

Two subunits A) inhibits proteins synthesis and is surrounded by B) binds to ceramics cell receptors- used in apoptosis

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24
Q

What is HIV?

A

Human immunodeficiency virus

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25
Q

How many strains of HIV are there?

A

2- HIV1&2: however HIV-1 has many subtypes due to mutations.

26
Q

What virus family does HIV belong to?

A

Lentivirus family

27
Q

Describe HIVs genome?

A

2 single stranded RNA molecules each bound by a reverse transcriptase

28
Q

HIVs genome is surrounded by a capsid with two layers. what are they made of?

A

Inner layer- p24

Outer layer- p17

29
Q

What proteins form HIVs viral envelope?

A

gp120 and gp41

30
Q

What does HIV gag protein do?

A

Produces gag precursor processes by viral protease. It then associated with the membrane attract 2 RNA copies and viral proteins before budding off into a virion

31
Q

What cells does HIV. Infect?

A

Cells that express CD4 glycoprotein. Eg: monocytes, helper T-cells and dendritic cells

32
Q

What are the two stages of viral infection?

A

Binding to the host cell and fusion with the membrane.

33
Q

What protein does HIV have that binds CD4?

A

gp120 protein

34
Q

What is the HIV lifecycle?

A

Binds CD4 via gp120. The nucleocapsid enters the cell and releases RNA & RTase produces DNA. Viral proteins translate from RNA. Assembly of RNA and protein into viral particles where the bud of the membrane.

35
Q

What is special between HIV and dendritic cells?

A

Dendritic cells can be hijacked and used to move around the body and to lymph nodes as they’re attract CD4 T-helpers- causes increased infection.

36
Q

What is HIVs Gp160?

A

It’s a glycoprotein trimer used to overcome fusion energy barriers.

37
Q

How does HIVs Gp160 protein work?

A

It cleaves into gp120 & gp41. gp120,binds CD4 receptor allowing binding to CXCR4/CCR5. gp41 becomes integral to both membranes

38
Q

What are M-trophic?

A

Use CCR5 receptor allows infection of T-helper, macrophages, monocytes and dendritic.

39
Q

What is T-tropic HIV?

A

Use CXCR4 can only infect T-helper cells

40
Q

What mutation can cause HIV resistance?

A

Homozygous for mutant CCR5 these individuals are resistant to infection of HIV.

41
Q

What does emergence of T-tropic signal?

A

Rapid progression of AIDs

42
Q

Why does HIV have a high mutation rate?

A

~10 mistakes per replication leading to a high mutation rate.

43
Q

What is latency in HIV?

A

Latentcy is the time between HIV infection and development of AIDs

44
Q

How does HIV hitch a ride to lymphnodes from dendritic cells?

A

Using a sialyllactose head on GM3 ganglioside (glycosphingolipid) exposed on HIV membrane is recognised by dendritic cells and takes up the virus

45
Q

What happens to serum antibodies in people with HIV?

A

They have increased serum antibodies and autobodies even though they have impaired antibody responses.

46
Q

What happens directly after HIV infection?

A

There is a period of rapid viral replication

47
Q

Why does HIV enter the latent phase?

A

Infection results in strong antibody response to gp120 and p24. Alongside a strong CD8 cytotoxic which eliminates 99% apart from 1% as a prophage entering latent phase

48
Q

Is the latent phase really latent?

A

No, there is a high level of viral replication known as viraemia

49
Q

What can viraemia tell us?

A

High levels of of viraemia means faster development of aids.
Low levels of viraemia means slower development of aids

50
Q

What give HIV higher chance of immunological survival?

A

It has a very high replication rate and can hide as a provirus
HIV also has a very high mutation rate so antigen aren’t recognised well

51
Q

How do you get CD4. T-cell loss?

A
  • HIV causes direct lysis
  • Infected cells have antigen on surface membrane so are killed by antibodies and complement
  • cytotoxic CD8 T-cells
52
Q

What molecule mediates apoptosis?

A

Capase-3

53
Q

What molecule mediates pyroptosis?

A

Capase-1

54
Q

What is pyroptosis?

A

A highly inflammatory form of lytic programmed cell death

55
Q

How does pyroptosis occur?

A

Inefficient reverse transcription leads to accumulation of viral DNA detected by DNA sensor IFI16 resulting in the inflammasome forming- causes activation of Capase-1 that causes pyroptosis

56
Q

What are the 3 categories of HIV drug used?

A
  • nucleoside analogue reverse transcriptase inhibitors
  • non-nucleoside analogue reverse transcriptase inhibitors
  • HIV protease inhibitors
57
Q

How do HIV Nucleoside analogue reverse transcriptase inhibitor drug work?

A

They lack a 3’-hydroxyl group in deoxyribose so cannot join the next nucleoside replication halts- called chain termination.

58
Q

How do HIV non-nucleoside reverse transcriptase inhibitors work?

A

They bind to reverse transcriptase inhibiting movement of protein domains that are needed to carry out DNA synthesis.

59
Q

How do HIV protease inhibitors work?

A

They inhibit the active site of reverse transcriptase used to leave precursor proteins preventing protein synthesis.

60
Q

What is the best treatment for HIV?

A

Combination treatment of all three as it can be very effective at reducing virus levels and increasing CD4 levels. However they can be quite toxic to humans so some can’t take the regime.

Immunology Infection And Inflammation (7 decks)

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