Attachment, Entry, Assembly and Exit (5,10) Flashcards

1
Q

How is the growth curve different between enveloped and non-enveloped viruses?

a. Non-enveloped viruses do not demonstrate a latent period
b. Enveloped viruses have a higher yield when they are intracellular
c. Intracellular viruses have a higher yield when non-enveloped and extracellular viruses have a higher yield when enveloped
d. The uncoating phase is only seen in enveloped viruses and has a low gradient on the curve

A

c. Intracellular viruses have a higher yield when non-enveloped and extracellular viruses have a higher yield when enveloped

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2
Q

What does it mean if P(0) = 0.02?

a. The multiplicity of infection is at 2%
b. 2% of cells are not infected
c. There is a 2% chance that any cell will become infected
d. There are 2 plaque forming units/cell

A

b. 2% of cells are not infected

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3
Q

What is not a method used by viruses to invade host cells?

a. Fusion and direct uncoating at the plasma membrane
b. Pinocytosis or phagocytosis
c. Endocytosis followed by uncoating within the endosome
d. Endocytosis followed by uncoating at the nuclear membrane

A

b. Pinocytosis or phagocytosis

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4
Q

What is NOT involved in the entry and uncoating of adenovirus?

a. The virus directly fuses with the host cell using CAR receptors and uncoats at the cell surface
b. When the endosome acidifies, the penton base is released and bursts the endosome so the capsid can be released
c. The adenovirus penton fibre interacts with intergrins recpetors called CAR to initiate RME
d. Once the capsid is released from the endosome, it travels to the nuclear pore using the host cell microtubule network

A

a. The virus directly fuses with the host cell using CAR receptors and uncoats at the cell surface

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5
Q

What is NOT involved in the entry and uncoating of Reovirus?

a. The capsid undergoes proteolysis in the endosome to produce the infectious subviral particle (ISVP)
b. ISVP proteins prevent endosome maturation and the virus can persist in the host
c. The outer capsid proteins bind cell receptors to mediate RME
d. ISVP proteins mediate membrane penetration

A

b. ISVP proteins prevent endosome maturation and the virus can persist in the host

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6
Q

What does not occur during entry of Influenza?

a. Envelope haemagglutinin molecules bind sialic acid on cell glycoproteins
b. Neuraminidase releases sialic acid and is part of the viral envelope
c. Endosome acidification is required so that the fusion domain of haemagluttinin can be exposed
d. The virus enters host cells by interacting with glycoprotein siali acid and directly fusing with the plasma membrane

A

d. The virus enters host cells by interacting with glycoprotein siali acid and directly fusing with the plasma membrane

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7
Q

What is CD46/SLAM?

a. A paramyxovirus ligand that reacts initiates fusion of the measles virus
b. A HIV-1 ligand that interacts with CD4 co-receptors during cell entry
c. The product of VP4 in Rotavirus following cleavage by trypsin
d. The flavivirus peptide that initiates membrane fusion following conformational change

A

a. A paramyxovirus ligand that reacts initiates fusion of the measles virus

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8
Q

What is the correct description for HIV-1 glycoproteins?

a. Gp120, gp41 and gp160 all exist as a trimer
b. Only gp160 can bind CD4
c. Gp160 is the precursor for gp41 and gp120
d. Gp41 is a surface protein and gp120 is a transmembrane protein

A

c. Gp160 is the precursor for gp41 and gp120

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9
Q

What happens during HIV entry? (put in order)
• Binding of gp120 to CCR causes conformational change in gp41 (transmembrane) and fusion peptide is inserted into membrane
• Gp120 (surface) binding to CD4 causes conformational change in gp120. Exposes binding site for chemokine coreceptor (CCR)
• HIV-1 envelope glycoproteins gp120-41 bind CD4

A
  • HIV-1 envelope glycoproteins gp120-41 bind CD4
  • Gp120 (surface) binding to CD4 causes conformational change in gp120. Exposes binding site for chemokine coreceptor (CCR)
  • Binding of gp120 to CCR causes conformational change in gp41 (transmembrane) and fusion peptide is inserted into membrane
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10
Q

What is used to determine is a virus infects a cell via endocytosis or direct fusion?

a. Genome sequencing and analysis
b. Exposing cells to a weak base to prevent endosome acidification
c. Electron microscopy
d. PCR for well-known fusion proteins such as SLAM, Gp120 and Gp41

A

b. Exposing cells to a weak base to prevent endosome acidification

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11
Q

• Initial binding of a virus is specific and the strongest form of attachment due to covalent protein-protein interactions.

A

F

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12
Q

• Virions may enter a cell by fusion, receptor mediated endocytosis or passive pinocystosis.

A

F

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13
Q

• Measles virus unocats by fusing their envelope with the cell plasma membrane.

A

T

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14
Q

• Poliovirus enters a cell after interaction between the CD155 receptor and capsid leads to a conformational change of the VP1 capsid protein.

A

T

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15
Q

• All reoviruses have a double shelled capsid except for rotavirus.

A

F

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16
Q

• It is common for enveloped viruses to enter in the endosome and rely on endosome acidification initiating a conformational change.

A

T

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17
Q

What is not a step in virus assembly shared by all viruses?

a. Form individual structural units of protein shell from one/several viral proteins
b. Selective nucleic acid packaging and other essential virion components
c. Envelope acquiring
d. Protein shell assembly, interactions between structural units

A

c. Envelope acquiring

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18
Q

What is not an issue to consider during virus assembly?

a. Some viruses require access to viral-encoded non-structural morphogenetic factors, such as chaperones
b. Proteins and nucleic acids must reach their correct location
c. Intracellular trafficking is essential
d. Virion components can be hard to locate when mixed up in the cytoplasm of non-compartmentalised eukaryotic cells

A

d. Virion components can be hard to locate when mixed up in the cytoplasm of non-compartmentalised eukaryotic cells

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19
Q

What is ψ?

a. Viral nucleic acid that has been distinguished from host cell DNA/RNA
b. Packaging signals in the viral genome
c. A morphogenetic chaperon required for virus assembly
d. The inverted repeat present in the HIV genome that aids in genome packaging

A

b. Packaging signals in the viral genome

20
Q

What is involved in the genome packaging of adenovirus?

a. The RNA genome is spliced and each mRNA is tagged with a specific packaging signal
b. A complex, repeating and overlapping packaging signal at the left IR and origin has enhancers to stimulate late transcription
c. The packaging signal at the right IR interacts with viral IV2A to stimulate early transcription
d. Because it has a dsDNA genome, it manipulates host cell machinery to selectively target viral proteins

A

b. A complex, repeating and overlapping packaging signal at the left IR and origin has enhancers to stimulate late transcription

21
Q

What is not involved in the packaging of the HIV genome?

a. Stem Loop 3 is only exposed in monomeric RNA which signals for packaging to occur
b. Gag NC mediates selective encapsidation of genome RNA during assembly
c. Ψ signals are in spliced regions so that only genomic RNA, and not mRNA, is packaged
d. The NC only binds to dimeric RNA that represents genomic HIV nucleic acid

A

a. Stem Loop 3 is only exposed in monomeric RNA which signals for packaging to occur

22
Q

What is not a way that virions can be assembled?

a. Association of individual monomeric proteins translated as separate components
b. From large polyprotein subunits refolded after proteolytic processing
c. With assistance of viral or cellular chaperon proteins for folding
d. Using scaffold proteins that bring components together and are incorporated into the mature particle

A

d. Using scaffold proteins that bring components together and are incorporated into the mature particle

23
Q

How does the virion assembly of SV40 and Adenovirus compare?

a. Both viruses require the chaperon protein L4
b. Adenovirus has spliced mRNAs that translate monomeric proteins
c. In adenovirus monomeric proteins assemble to penton units first as homo-multimers
d. Sv40 has Hexon units made from trimers of papovaviral protein II

A

c. In adenovirus monomeric proteins assemble to penton units first as homo-multimers

24
Q

What is NOT involved in the encapsidation of Herpes Virus?

a. Genome replication makes concatomers
b. Packaging signals, pac1 pac2 are recognised so viral DNA can be cleaved within DR1
c. One end of the genome is recognised by the pac proteins before cleavage and encapsidation
d. Scaffold proteins are involved and a protease is required to finalise the viral structure

A

c. One end of the genome is recognised by the pac proteins before cleavage and encapsidation

25
Q

What happens during the assembly and encapsidation of poliovirus?

a. The process relies on the action of the L4 chaperone
b. Proteolytic cleavage and correct protein folding is essential
c. VP2 and VP4 are cleaved to form VP0
d. The 5s structural unit is made up of 3CDpro subunits

A

b. Proteolytic cleavage and correct protein folding is essential

26
Q

Put the sequence of poliovirus maturation and exit in order

  1. Particles assemble in cytoplasm (incompletely cleaved, retain VP0)
  2. Cell dies, virus released
  3. RNA genome replication in cytoplasm in smooth ER
  4. Package viral RNA and form non-infectious virion
  5. Final cleavage of VP0 to VP4 and 2 leads to infectious virus
A
  1. RNA genome replication in cytoplasm in smooth ER
  2. Particles assemble in cytoplasm (incompletely cleaved, retain VP0)
  3. Package viral RNA and form non-infectious virion
  4. Final cleavage of VP0 to VP4 and 2 leads to infectious virus
  5. Cell dies, virus released
27
Q

Which virus is huge and capable of inducing cell lysis to release viral particles?

a. Adenovirus
b. Poxvirus
c. Poliovirus
d. Mimivirus

A

d. Mimivirus

28
Q

What best describes a strategy used in the assembly of an enveloped virus?

a. Alphavirus depends on envelope glycoproteins and capsid
b. Coronavirus requires the internal matrix and capsid proteins to drive budding
c. Retrovirus budding is driven by envelope proteins
d. Picornavirus budding is driven by matrix proteins and RNP for efficiency

A

a. Alphavirus depends on envelope glycoproteins and capsid

29
Q

What is false about the targeting of virus glycoproteins and enveloped virus assembly?

a. BFA can block viral infection by blocking ER to Golgi transport
b. Glycoproteins with retention motifs are destined for the ER or Golgi
c. Glycoproteins can only target the plasma membrane due to the thickness of their transmembrane domain
d. Glycoproteins require specific processing in the ER and Golgi

A

c. Glycoproteins can only target the plasma membrane due to the thickness of their transmembrane domain

30
Q

What is not involved in the assembly of influenza virus?

a. Mature HA, NA and M2 are made in the nucleus
b. M1 binds RNP and prevents further transcription and NEP binds the complex via M1
c. When the membrane pinches off, NA cleaves sialic acid and the virion is released
d. Glycoproteins concentrate in the PM and are bound by M1 which initiates budding

A

a. Mature HA, NA and M2 are made in the nucleus

31
Q

What would happen if furin was not functional in a cell infected with Flavivirus?

a. The virus would fail to exit the recycling endosome
b. prM would not be cleaved to M and the virus would not mature
c. The viral envelope would fuse with cell envelopes during its transport
d. pH would not have a role in maturation of the virion

A

b. prM would not be cleaved to M and the virus would not mature

32
Q

What is false about the assembly and maturation of HIV?

a. The virus assembles at the plasma membrane due to the accumulation of TM-SU, myr-MA-GAG into lipid rafts
b. HIV Gag-MA is modified by myristoylation and phosphorylation
c. TM-SU has RNA binding sites (basic) and two zinc-finger motifs
d. Furin cleavage releases Tm and SU from env precursor

A

c. TM-SU has RNA binding sites (basic) and two zinc-finger motifs

33
Q

How does vaccina exit the cell?

a. It travels to the edge of the cell via actin
b. It exits the cell by hijacking microtubules and using them as propeller like tails
c. It uses the secretory network to exit via exocytosis
d. It utilises microtubules and actin

A

d. It utilises microtubules and actin

34
Q

• The adenovirus packaging signals is in spliced regions so only genomic RNA is packaged as opposed to mRNAs.

A

F (HIV)

35
Q

• New DNA virus particles are often released after a cell breaks down due to the toxic effects of viral proteins.

A

T

36
Q

• Most DNA viruses assemble in the nucleus.

A

T

37
Q

• SV40 Vp1,2,3 can enter the nucleus due to the action of the L4 chaperone.

A

F

38
Q

• Adenovirus hexon proteins lack a NLS but still enter the nucleus due to the action of a chaperon.

A

T

39
Q

• Nuclear localisation signals have a high amount of basic charged AAs which can bind nucleic acid.

A

T

40
Q

• Membrane bound glycoproteins are translated on free ribosomes.

A

F

41
Q

• Ribosomes dock to the ER if the translated protein has a N terminal 20 AA hydrophilic sequence.

A

F

42
Q

• Enveloped viruses bud from the cell membrane so that the cell membrane forms the coat with viral proteins and the nucleocapsid is inside.

A

T

43
Q

• The movement of viral proteins and particles with the cell is independent of host cell processes.

A

F

44
Q

• Flavivirus exits the cell by exocytosis after passing through the ER, Golgi and Recycling Endosome.

A

T

45
Q

• During HIV maturation, Gag myristoylation promotes binding to phosphatidylinositol-(4,5)-bisphosphate which is only found in the PM.

A

T

46
Q

• When exiting polarised cells, viruses that exit apically come into contact with blood, lymph and nerves and can spread systemically.

A

F