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m2m > Module 3: COVID19 > Flashcards

Module 3: COVID19 Flashcards

1
Q

DEFINE INFECTion control & aseptic technique

A
  1. infection control = prevent & minimise cross infection
  2. aseptic technique = procedure & equipment to prevent transfer of microorganisms
    - underpins infectious control measures
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2
Q

what are 3 ways infections can be spread

A

direct contact, aerosol & equipment

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3
Q

what are the infection control measures (5)

A
  1. contain infection to patient
    - isolate infected people
  2. protect susceptible individuals
    - protect high risk patients (esp in hospitals where doctors need to wear proper masks, ppe)
  3. reduce no. of susceptible individuals
  4. reduce contact between infected & susceptible individuals
    - lock down & distancing
  5. reduce no. of days of infectivity
  6. prevnting transmission from source, formites & droplet/aersols

from source: masks, social distancing, hand wash

from formites: disinfection & hygiene, lockdown (to reduce concentration of ppl in public)

from aersols & droplets (maska, cover cough/sneeze)

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4
Q

how is covid transmitted

A
  1. direct contact = skin, bodily fluids, mucous membranes
  2. indirect contact = through formites (objects that carry virus)
  3. droplets = sneeze/cough -virus particles drop to the group/ surface of object, usually travels 1m or less
  4. Airborne = virus small enough particles that
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5
Q

2 types of droplets

A
  1. smaller droplet nuclei = contain less infectious agent (<5um), travel further (>1m), persist in air
  2. larger droplets = contain more infectous agent (>5um), travel less than 1m
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6
Q

define the R0 value

A

no. of people an infected person can infect

R>1 = epidemic (infection spreads rapidly)
R=1 endemic (each infected person infects one other person, seasonal flu)
R<1 disease eventually disapears

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7
Q

what factors determine inactivation and what does can this influence?

A

inactivation depends on:

  1. temperature
  2. moisutre
  3. viral structure
  • enveloped = outer lipid bilayer, as it leaves host cell it takes some lipid membrane with it = more easy to neutralise (detergent)
  • non-enveloped = has protein capsids, more tolerant of environemntal conditions than enveloped virus
    4. initial level of virus (amount of virus remaining to transmit)
  1. type of surface (non porous vs porous)
    - porous surface (less than 4 hrs on copper, less than 24 hrs on cardboad = sustain virus for less time than non porous (up to 72 hrs on plastic / stainless steel)

these factors determine

  1. survival on surface (initial level of contamination + type o fsurface)
  2. susceptibility to disinfection
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8
Q

describe S1 and S2

A

S1 receptor binding = the polyarginine cleave site of the genome

  • cleavage site to allow receptor to bind
  • S1 domain of spike binds to variety of different host receptors –> cause viral attachement
  • Cleavage occurs DURING VIRAL SYNTHESIS ( as viral particles assemble, before virus binds to receptor ) AND during exit ( so that the virus can bind to a new cell)

S2 membrane fusion
- must be cleaved AFTER virus binds receptor (during viral entry) –> cleavage activates S2 –> causes structural rearrangement that exposes hydrophobic domain that insert into the membarne (plasma/ endosome) –> cause further structural changes that bring the virus + host membrane together –> ends up with fusion pore

as virus exits host cell on its way out, it will INACTIVATE S2 so that virus will not refuse with an initailly infected cell –> reactivates after virus binds to receptor of new cell

2 cleavage proteases cleave:
1) TMPRSS2 = extracellular cleavage protease (if virus enters via direct entry thorugh plasma m)

2) Cathepsin L = intracellular cleavage protease (if virus enters via endocytosis into endosome)

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9
Q

HOW IS SPIKE GENOME DIFFERENT IN COV2 COMPARED TO COV1

A

1) in sars 2, there is a POLYBASIC CLEAVAGE SITE= cleaved by FURIN
- furin = is present in most cells across diff species
- sar2 is able to infecte MORE + BROADER RANGER OF CELLS

2) sars 2 genome of SPIKE PROTEIN= shows HIGHER AFFINITY to receptors

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10
Q

why does covid 2 have higher transmissibility than cov1?

A

1) ASYMPTOMATIC TRANSMISSION= high shedding beofre symptoms manifest
- dont know ur infected cos u dont have symptoms. but you are shedding viral particles = more likely infect others

  1. high shedding at UPPER RESPIRATORY TRACT = easier to spread
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11
Q

what is the CORONA VIRUS replication process

A

when virus enters host it will first transcribe the OPEN READING FRAMES ORF 1A+1B –> these POLYPROTEINS PP1A+PP1B –> polyproteins are cleaved into NON STRUCTURAL PROTEINS nsp that:

1) combine to form RNA DEPENDANT RNA POLYMERASE
2) recruit DMV DOUBLE MEMBRANE VESICLES (highly modified membranes)

DMV will encase replication machinery (viral dsRNA, rdrp, viral proteins), its purpose is for:

1) fast replication of viral proteins (since its within a confined space)
2) to hide viral dsRNA + viral protiens –> to evade immune system

within the dmv: RDRP will SKIP THE ORF, transcribe bind nested-sub genomic RNA–> transcribe sub-genomic RNA into sub-genomic PROTEINS:

1) structural proteins (more virus, env, nucleocapsid)
2) accessory proteins
3) other proteins that hlep produce the membrane chain

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12
Q

what skips the ORF and why?

A

the RdRp RNA dependant rna polymerase skips the ORF because replicase (rdrp) is already made.so theres no need to make more rdrp

  • Orf transcribes non-structural proteins such as rdrp replicase
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13
Q

where is ace2 expressed

A
  • there is very limited expression of AC2
    and very limited CO-EXPRESSION of ACe2 with TMPRSS2 (Serine protease that cleaves S domains on spike protein)

airways:

  • upper nasal cavity
  • goblet cells
  • ciliated cells

lower repsiratory cells:

  • ciliated/basal cells
  • club cells

alveolar parenchyma
- pneumocytes (tyep 1 and 2)

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14
Q

why is diarrhoea a symptom of corona?

A

whereever there is co-expression of ACE2 receptor + TMPRSS2 serine protease–> it is more likely that when someone is infected by corona, they will see pathogenesis at these sites

  • liver
  • ileum
  • colon
  • ACE2 receptor on host cells is what corona virus binds to
  • TMPRSS2 serine protease= is what allows virus to bind to the receptor, fuse with the membrane
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15
Q

what is the pathogenesis of spike - ace2 receptor interaction?

A

spike binds to ace2 receptor on host cell –> takes ace2 with it inside cell –> causes down regulation of ace2 receptor, which causes angiotensin 2 accumulation (since ace2 converts ang2–> ang1-7 inactive form) –> more ang2 will bind to AT1 receptor –> causing vasoconstriction + hypertension

  • responsible for acute lung injury
  • adverse myocardial remodelling
  • vasoconstriction –> hypertension
  • vascular permeability
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16
Q

types of vaccines against corona?

A

1) RNA vaccines
2) DNA vaccines
3) Recombinant protein vaccines
4) Vectored vaccines
5) Inactivated vaccines
6) Live attenuated vaccines
7) Non-replicative virus-like particle vaccines

17
Q

why arent nabs always protective

A
  1. infection of macrophages through differenet uptake pathway of virus
  2. macrophages can cause NUCELOCAPSID to tranfer virus into other tissues
18
Q

What are the effect sof high virus level?

A

high virus causes lots of ACE2 receptors to become activated

  • ACE2 receptors are IFN stimulated genes in human airway epithelial cells
  • when lots of IFN present due to high virus present–> causes upregulation of ACE2 receptors in cells that might not usually express ACE2 = provides MORE targets for HIV to bind & infect
19
Q

effects of cytokine storm?

A 
corona infected cell will activated macrophages, monocytes + dendritic cell --> all produce IL6 which further causes CYTOKINE STORM:
(III VLH MD)
it increases: 
1) Il6 &amp; others
2) Immune activation
3) Inflammatory macrophages + neutrophils
4) Vascular permeability
5) Liver + kidney damage
6) Hypoxia >80% sat
7) Mechanical ventilation
8) death
20
Q

what are the potential treatment options?

A
  1. produce soluble ACE2
  2. produce antibodies that bind to receptor binding domain of Spike proteins
  3. Chloroquine + hydroxyghloroquine
21
Q

what are the effects of chloroquine + hydroxychloroquine

A
  1. CQ can reduce glycosylation of ACE2
  2. CQ can dampen cytokine storm by blocking production of proinflammatory cytokines (IL6)
  3. CQ can raise pH of endosome = by accumulating inside lysosomes = so its less ideal environemnt for HIV virus to enter + leave
  4. HCQ affects cleavage sthat are PH dependant
22
Q

what are vaccine targets for corona/ therapeutic options for sars?

A

SSAC:

  1. Serine protease inhibitors
    - prevent proteases (tmprss2, cathepsin L) from cleaving S1/S2 sites –> prevents receptor binding + membrane fusion
  2. soluble ace2 receptor
    - block spike protein from bidning = prevent cell infection
    - must be soluble so that transmembrane ace2 receptor sitll able to carry out normal fangiotenisin pathway
  3. NEUTRALISING Antibodies against RECEPTOR BINDING DOMAIN of spike protein
    1) RNA vaccines
    2) DNA vaccines
    3) Recombinant protein vaccines
    4) Live attenuated vaccines
    5) Inactivated vaccines
    6) Vectored vaccines
    7) Non-replicative virus-like particle vaccines
  4. Chloroquine + hydroxychloroquine

1) CQ = reduce glycosylation of ACE2 to:
i. reduce spike-ace 2 binding
ii. can impede function of spike protein on the virus that is leaving the cell = impede spike function

2) CQ= can block production of pro-inflammatory cytokiens (IL6)
- reduce cytokine storm

3) CQ= increase pH inside endosome = to prevent viral entry / exit
4) HCQ = also affects cleavages that are pH dependant

23
Q

compare proteins between sars 1 and sars 2

A

sars 1 and sars 2 have 80-90% homology, except for 3 main proteins

  1. nsp3 = 76% homology
    - block host innate immune system + promote cytokien expression
24
Q

how does IFN signalling affect disease pathology

A

EARLY IFN RESPONSE = MILD CLINICAL DISEASE

  1. low virus titre = even though IFN is produced and causes ACE2 upregulation= there isnt enough virus that will actually bind to ACE2 receptor
    - may be high virus replicating within dmv inside cells, but not out in the blood where it can bind to ace2 recpetors and cause infection
  2. Regulated INFLAMMATION = IFN produced will be able to recurit monocytes / macropahges to control infection, without there being over-immune activation
  3. mild clinical disease

DELAYED IFN RESPONSE = SEVERE CLINICAL DISEASE

  • high virus titre builds up, so that by the time IFN is produced, ifn will recruit so many monocytes & macrophages that it becomes dysregulated, and cant clear the virus properly
    1) dysregualted IMM = so mnuch virus causing IFN to recruit as many monocytes/macrophages as possible= but due to magnitude of virus, it cant be cleared. instead monocytes/macrophages detect viral RNA via TLR and engulf the virus infected cells , move around body –> carry virus around body –> infect more cells
  • also will stimulate lots of non neutralising antibdoies= that also carry virus around body
    2) Lung immunopathology= since IFN upregulates ACE2 expression –> causes more virus to bind to cells –> ang2 accumulates –> binds AT1 receptor –> causes acute lung injury, adverse myocardial remodelling, vasoconstriction , vascular permeability
    3) lethal pneumonia

NO IFN RESPONSE = mild clinical disease

1) regulated IMM= no IFN so it wont contribute to monocyte / macrophage recruitment.
2) no lung immunopathology = because IFN is not present = wont upregulate ACE2 expression = wont cause angiotenin pathway to go down
3) mild clinical disease

25
Q

Why do older people whoa re more prone to severe disease, have HIGH levles of Nabs?

A

they most likely have a delayed IFN response = meaning that by the time IFN have been made there is already a HIGH VIRUS TITRE.

causes
1) dysregulated IMM + inflammation
so much IFN will recruit more monocytes/macrophages in an uncontrolled manner
- high virus conc causes IFN to upregulate expression of ACE2 = cause = virus can infect more cells
- macrophages + monocytes will detect viral RNA by their TLR receptors on endosome= cause them to take up viral RNA & express viral proteins –> move around body & carry virus around body
2) lung immunopathology
- due to upregualtion of ACE2= increase ang2 bidning to at1 receptor = causing acute lung injury
3) lethal pneumonia

m2m (4 decks)

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