Convince the expert, host-virus interactions Flashcards

1
Q

How does Covid evade the type I IFN responses?

A

Covid can interupt the TLR’s, suppress the downstream signallinh andaler the function of IFN-stimulated genes.

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2
Q

How can covid induce the cytokine storm?

A

Its attachment receptor is te ACE2 receptor, by binding to this and entering the cell, ACE2 levels will drop. ACE2 usually down regulates the activity of NF-kB by interfering with angiotensin II downstream signalling. This does not happen anymore and inflammatory cytokines will keep being produced. Leukocytes are attracted to this and will also produed inflammatory cytokines. This results in a positive feedback loop, thus a cytokine storm

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3
Q

How do vaccines help prevent transmission in covid?

A

We will get less sick > less coughing and sneezing > it is neutralised faster> virions that we cough or sneeze out can already be neutralised by antibodies by then.

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4
Q

What are the 5 mechanisms of how Sars-cov2 viruses can escape binding by antibodies?

A
  1. alteration epitope by aminoacid substitution
  2. increasing receptor-binding avidity, this heightens the interaction between glycoproteins and cellular receptors
  3. changes in glycosylation, that is the shield of the epitopes that prevents antibody binding
  4. deletion and insertion in amino acids in the epitope
  5. allosteric structural effects. this is outside the epitope sequence but may be able to change the structure of the epitope itself
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5
Q

What is the mutation of Sars on S477N?

A
  • located on position 477 on spike protein.
  • this heightens the affinity for the ACE2 receptor, thus easier to bind
  • resistant to neutralisation by entire pantal receptor binding.
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6
Q

How can HIV-1 alter the NF-kB pathway?

A

in normal cases, NF-kB induces inflammatory cytokines. But HIV-1 can also use NF-kB to induce efficient transcription of HIV-1.

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7
Q

What is the difference in the traditional model and the current model of HIV-1 replication?

A

In traditional models, HIV-1 uncoats their DNA the moment they are in the cell. In theory they shouldthen be able to activate the TLR’s.

However, current models state that it happens when the virion is in the nucleus. This impacts the way on how HIV-1 works. in this situation. TLR’s cannot signal it because it is not uncoated yet.

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8
Q

What cells are the target cells for HIV and what are the consequences of it?

A
  • CD4 cells are the target, the consequences is that the adaptive immune system is essentially knocked out. B-cells will not mature and isotype switch, and CD8 cells will not/barely get activated. On top of that, because of the inactive immune system, commensals can become pathogenic while normally they do not have the chance.
    same goes for cancer
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9
Q

What are the stages of HIV?

A
  • infection in mucosal layer (hours)
  • local expansion (3-4 days)
  • dissemination to lymphatic tissues (days-weeks)
  • local proliferation (1-2 weeks)
  • partial immune control ( weeks, months years)
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10
Q

How does the ART work(what parts are they inhibiting?)

A
  • fusion
  • integrasee
  • reverse transcriptase
  • protease
  • attachement of the co receptors (CD4 and or CCR/CXC4)
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11
Q

Is it inevitable to transmit HIV during intercourse?

A

No, the partner can be protected even without physical barrier. If the host is on fully suppressed load on antiretroviral treatment then the risk is 96% reduced. If the viral load is below detectable levels, than transmission does not occur at all

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