membrane remodelling Flashcards

1
Q

Where is membrane remodelling by viruses involved in?

A
  • infection
  • genome replication
  • egress
  • cell to cell spread
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2
Q

Which membranes are remodelled by which viruses?

A

ER:
- Polio
- HCV
- Corona

ER/Golgi/intermediate
- kunjin virus

Lysome/PM
- Rubella virus
- alpha virus

Mitochondria
- flock house virus

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3
Q

How can membranous bending be generated? Name Examples

A

By proteins via different mechanisms:
- membrane protein shape
- amphiphatic helix insertion !
- membrane protein oligimerization
- scaffolding by peripheral proteins
- lipid composition

Examples:
- clathrin coated vesicles
- coatamer proteins COPI and COPII

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4
Q

How can nidovirales induce the formation of double membrane vesicles?

A

different models:
1. protrusion and detachment model:
-ER cisterna start to bend, pinches off and seals
2. double buddig model: a single membrane vesicles buds into the lumen of the ER and then buds out again

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5
Q

where do SARS Cov 2 virons budd and assemble?

A

at the ERGIC membrane

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6
Q

What induces autophagy and how does it work?

A
  • Reaction to stress, starvation and ifection
  • compasing of cytoplasmatic parts with sickle shaped vacoules
  • fusion with lysosomes
  • content degradation in autophagosomes
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7
Q

How many autophagy related gene s (Atg) are there? What happens if ATG12 and lC3 are knocked down durin Poliovirus infection

A

27 atg
– > knock down does not inhibit replication of polio virus but agress of new viruses

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8
Q

What induces membrane concativity?

A

oligomeric viral membrane proteins

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9
Q

Do all + Strand RNA viruses modify intracellular mmebrane systems or generate vesicle like structues or vesicles networks? Why?

A

yes, because RNA replication always takes place at membranes

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10
Q

What are the functional properties of remodelling of membranes by + Strand RNA viruses?

A
  • shielding of dsRNA intermediates from the innate immune system
  • resistamce against RNases and proteases
  • high local concentration of viral components
  • contact with ER components of the cell
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11
Q

which protein plays a role in flock house remodelling of the mitochondrial outer membrane?

A

ptnA

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12
Q

Where does the alphavirus chikungunya virus replicate its genome? Which viral proteins play a role?

A
  • in membrane spherules at the plasma membrane
  • nsp1 is base for assembly of larger protein complex
  • nsp1 recruits nsp2
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13
Q

Where does the energy for membrane remodelling by chikungunya virus come from?

A

from the released energy during RNA polymerization

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14
Q

How are progeny + strand RNA genomes released from replication vesicles? To what is it comparable?

A

RNA synthesis takes place close the the pore structure for the release of this RNA into the cytoplasm –> comparable to dsRNA synthesis which takes place in cores close to the exit channels

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15
Q

Describe the dengue virus vesicles. Where does budding occur?

A
  • ER derived
  • netwotk of convoluted membranes
  • invagination of ER membranes
  • have pores
  • look like nests
  • budding of virus particles on ER membranes opposed to pores –> budding occurs into the ER
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16
Q

Describe HCV rearrangements in HCV infected cells

A
  • derived from ER
  • vesicles are protrusions of the ER membrane
  • membranous webs consisting of single and double membrane vesicles
  • vesices are frequently connected to the ER membrane via a neck like structure
17
Q

compare dengue and HCV membrane remodelling

A

both form vesicles derived from the ER but
- dengue: invaginations
- HCV: protrusions

18
Q

describe the envelopment and cell egress of herpes viruses

A
  • two proteins UL34 and UL31 enable the stride of the capsid through the nuclear membrane into the ER
  • nuclear membrane istaken along as an envelope but this is lost during egress out of the ER
  • entry of capsid into golgi –> envelopment with golgi membrane stays
  • egress out of golgi via secretory vesicles leads to a second lipid envelope which is lost during the egress at the PM
19
Q

where does herpes virus gets it envelope from?

20
Q

Name mechanism through which cell-cell communication works

A
  • synapses
  • cytonemes
  • gap junctions
  • tunneling nanotubes
21
Q

can filopodia be abused by viruses?

22
Q

Give an explanation why the time scale of spreas is not in line with speed of replication in vaccinia virus

A

due to selective infection of uninfected cells –> new particles are bounced off and onto neighboring cell via actin tail formation and membrane protrusions triggered by virus particles (A33 and A36 viral proteins)

–> optimal efficiency for viral spread

23
Q

How do Poxvirus, HIV, MLV, ASFV, CMV and RSV do cell- to cell spread?

A

Pox: projection on actin tails
HIV: virological synapses, nanotubes
MLV: captur of filopodia
ASFV: induction of filopodia
CMV: cell to cell fusion
RSV: syncytium formation

24
Q

What role do FAST proteins play in reoviurs encoded cell-cell fusion machinery for viral spread via formation of syncytia?

A
  • is a NSP (so not in virion)
  • mediate only the step of fusion
  • only interact with membranes but not adhesion
  • active actin remodelling required
25
Q

Name modes for viral spread from cell to cell and give example viruses

A
  1. membrane fusions, synctia formation: Herpes, retro
  2. basolateral budding between tight junctions: herpes
  3. budding into synpatic cleft: herpes, rhabdo, paramyxo
  4. virus induced actin containing membrane structures carry virions into adjoining cell: murine leukemia virus
  5. actin containing nanotubes for transport into adjoining cells: HIV
  6. virological synpases
26
Q

Which virus can induce membrane bdriges between cells? How?

A

retroviruses via contact between viral coating proteins in filopodia and cellular receptor in the target membrane