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MVST1B BOD > L18 - GL Smith - PRIONS, emerging viruses & HIV > Flashcards

L18 - GL Smith - PRIONS, emerging viruses & HIV Flashcards

1
Q

what are prions?

A

infection proteins

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2
Q

prions causes diseases called?

A

transmissible

spongiform encephalopathies (TSEs)

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3
Q

describe transmissible spongiform encephalopathies (TSEs)

A

– Chronic, progressive, neurodegenerative

diseases, vacuoles in brain

– Infect both man and animals

– Invariantly fatal

– May take decades to develop

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4
Q

what does this picture show

A

prion infection in the brain

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5
Q

4 examples of prion diseases

A

Scrapie in sheep.

Kuru in the Fore tribes in Papua New Guinea, transmitted by cannibalism.

Creutzfeldt-Jakob disease (CJD) and variant CJD (vCJD) in humans.

Bovine spongiform encephalopathy (BSE) in cattle (also called mad cow disease)

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6
Q

Epidemic nature of Kuru suggested an infectious agent: transmitted by ____

A

Epidemic nature of Kuru suggested an infectious agent: transmitted by cannibalism

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7
Q

describe how te prion protein can cause srapie in sheeps?

A

abnormal conformation cannot be broken down by proteases = accumulation in neural tissue = amyloid plaques

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8
Q

Conversion of PrPc (cellular) to PrPSc (scrapie)

A
  • Spontaneous
  • Promoted by PrPSc

• Genetic - specific amino acid changes make the conversion easier

misfolded PrP catalyses the conversion

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9
Q

Prion diseases may occur following…

A

Prion diseases may occur following ingestion of infected material.

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10
Q

what caused the UK BSE epidemic

A

Caused by feeding cattle meat and bone meal (MBM) contaminated with prions from scrapie-infected sheep

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11
Q

can BSE trasmit to man?

A

yep

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12
Q

most common TSE in man?

A

CJD. (Creutzfeldt-Jakob disease)

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13
Q

whta is Creutzfeldt-Jakob disease likely caused by?

A

eating infected meat

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14
Q

how do we detect prions

A

no adaptive immune response to the abnormal form of the PrP, so no immunological evidence of exposure.

there are mAbs that detect PrPSc

Infectious prions can be detected by bio-assay:

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15
Q

describe scrapie in sheep

A
  • pre-clinical phase - infectious material firt associated with the gut lymphoid tissue
  • spreads to peripheral lymphnodes (haematogenic dissemination)
  • accumualtes in the CNS

breed geneticallyresistantflocks in UK

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16
Q

describe the surfcae proteins of SARSCOV2

A

prominent surface spikes – hence the name “corona”virus – each representing a trimer of the spike (S) protein

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17
Q

genomes of SARSCOV2

A

+ve ssRNA genomes: the largest for animal RNA viruses

29.9Kb

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18
Q

describe the role of NSP14 and 10 in sars cov 2

A

The non-structural protein (nsp) nsp14 (an exonuclease, ExoN) and nsp10, detect and excise 3’ nucleotide mismatches.

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19
Q

Does SARSVOC2 have proofreading capcity

A

yep - like other RNA viruses with genomes ovefr 20kb

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20
Q

SARSCOV2 most variable gene?

A

spike proteins

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21
Q

describe spike protein S

A

Spike (S) protein. The S protein forms homotrimers on the virion surface and mediates i) binding to target cells via the angiotensin converting enzyme II (ACE-2), and ii) membrane fusion. It is also the target of neutralising antibodies.

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22
Q

describe how S spike protein is cleaved to mediate membrane fusion (SARSCOV2)

A

The S protein is cleaved via cellular proteases into S1 and S2 subunits, which together represent one monomer of each trimer.

Cleavage is essential for the S protein to mediate virus entry.

Subunit S1 contains the receptor-binding domain (RBD) and S2 is needed for membrane fusion.

The S protein is the most variable protein between related CoVs, particularly in S1 within the RBD.

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23
Q

describe the disease caused by SARSSCOV2

A

asymptomatic in most people

excessiv pulmonary inflammation - loss of lung function

fatality - 0.3%

24
Q

give 6 risk factors of SARSCOV2

A

Age : the disease severity increases steeply over 65 yrs

Obesity: clinical obesity increases severity

Hypertension

Diabetes

Chronic lung conditions, e.g. asthma and chronic obstructive pulmonary disease (COPD)

Sex: males are more susceptible that females

25
Q

prevention methods of SARSCOV@

A

Social distancing

Wearing personal protective equipment (PPE) such as face masks

Hand washing

Quarantine of those infected and the contacts of those infected, including track and trace

+ VACCINE

26
Q

3drugs used for COVID

A

Dexamethasone

Remdesivir

mAbs

27
Q

how does dexamethasone increase COVID survival?

A

low doses during severe COVID-19 gives increased survival. This anti- inflammatory drug reduces lung inflammation and so may improve lung function.

28
Q

how does Remdesivir increase COVID survival

A

this is an inhibitor of the virus RNA-dependent RNA polymerase (RdRp).

It is given as a monophosphate pro-drug that is converted into a ribonucleoside triphosphate analogue to inhibit the virus RdRp. It can hasten recovery. May cause liver toxicity.

29
Q

how can mABs hel COVId recovery?

A

directed against the S protein

30
Q

if no drugs - whats the outcome for HIV?

A

Without drugs death is the outcome.

31
Q

is HIV increasing?

A

Yes. every 10 deaths = 24 new cases

32
Q

HIV is a retrovirus and belongs to the sub- family called ________. These viruses have more ______ genomes than the standard retrovirus, and cause slow infections.

A

HIV is a retrovirus and belongs to the sub- family called lentiviruses. These viruses have more complex genomes than the standard retrovirus, and cause slow infections.

33
Q

The HIV capsid is cone-shaped, composed of gag ___, and surrounded by an envelope with env proteins ____ and ___ (derived by cleavage of a precursor gp160).

A

The HIV capsid is cone-shaped, composed of gag p24, and surrounded by an envelope with env proteins gp120 and gp41 (derived by cleavage of a precursor gp160).

34
Q

what resticts antibody access for HIV

A

gp120 is heavily glycosylated and this glycan shield restricts access by neutralising antibody.

35
Q

describe HIVs genome

A
36
Q

prupose of the tRNA in the HIV genome?

A

prime reverse transcriptase

37
Q

The provirus structure differs from the RNA genome. At each terminus there is a …

A

The provirus structure differs from the RNA genome. At each terminus there is a long terminal repeat (LTR) (see also Figure 51).

38
Q

what do tat and rev proteins do in HIVinfections?

A

The tat and rev proteins regulate the switch to expression of the capsid and envelope proteins later during infection

39
Q

what does vpu do in HIV?

A

Vpu is multi-functional: it down-regulates CD4 (the HIV

receptor) and blocks NF-κB signalling to restrict innate immunity.

40
Q

describe HIV transmission

A

Transmission: sexual, intravenous drug abuse, mother to baby, contaminated blood products

41
Q

describe how HIV gains access to cells

A
42
Q

is CD4 sufficeint for HIV binding?

A

no - coreceptor needed

43
Q

HIV gene expression requires transcription of the provirus by host…

A

HIV gene expression requires transcription of the provirus by host DNA-dependent RNA polymerase II

44
Q

how is HIV released from the cell

A

HIV buds through the plasma membrane to release new virus particles. The electron micrograph shows an HIV particle almost detached from the infected cell.

does not kill the cell: but Eventually the cell may be recognised and destroyed by CD8+ CTL.

45
Q

how can HIV be latent?

A

HIV infection may be latent. Here the provirus is not transcribed, so no virus proteins are expressed and the cell cannot be detected by CD8+ CTL or antibody. Latently-infected cells provide a reservoir of HIV genomes that can re-seed infection and are the main reason why HIV infection is very hard to eliminate: even good drugs that block virus replication are ineffective because their targets are not expressed.

46
Q

describe:

A

After infection HIV replicates and induces an HIV-specific CTL response.

These CTL recognise and clear HIV-infected CD4+ cells, causing a transient drop in the CD4+ cell count.

However, as the level of infected cells is controlled by CTL and free virus particles are removed by antibody, the CD4+ cell count recovers.

The patient is then infected but may remain largely asymptomatic

virus continues to replicate - controlled by CD8 CTL.

CD4 cells depleat

less T cell help

= immmunodeficiency

oppertunistic infection = death

47
Q

does HLA haplotype have an effect on HIV?

A

Heterozygous carriers of certain HLA haplotypes, such as B27 and B57, have better prognosis after HIV infection.

48
Q

is there a HIV vaccine?

A

no

49
Q

is HIV highly mutatable?

A

yes because of its error prone reverse transcriptase, and it is estimated that in an HIV-infected patient up to 106 different mutant viruses are produced each day.

50
Q

how do we treat HIV

A

anti retro viral dtugs

51
Q

describe Azidothymidine

A

a thymidine analogue that is used against HIV. AZT is phosphorylated to the NTP by cellular kinases and is incorporated into the virus DNA by reverse transcriptase. Incorporation terminates chain growth. (no 3’ OH group)

Dideoxycytidine and dideoxyinosine, 3TC (lamivudine) are other chain terminating nucleoside analogues.

52
Q

how do Ritonavir, saquinovir, indinavir work?

A

The gag and gag-pol proteins are translated as a polyprotein that is cleaved by a virus protease during virion maturation to yield the capsid proteins and pol.

Several protease inhibitors have been developed that inhibit the HIV protease, but not host proteases.

These drugs prevent the completion of virus assembly

53
Q

is HIB highly mutable?

A

yes

54
Q

what is HAART

A

Highly active anti-retroviral therapy (HAART)

give multiple drugs simultaneously making it much more difficult for the virus to mutate to acquire resistance to all the drugs at once.

55
Q

fat

A

mamba

56
Q
A

MVST1B BOD (21 decks)

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