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MIC 430 > Lec 7: Assembly & Exit > Flashcards

Lec 7: Assembly & Exit Flashcards

1
Q

Nucleocapsid assembly: (4)

A
  1. ) Helical viruses
  2. ) Icosahedral viruses
  3. ) Genome packaging
  4. ) Assembly mechanisms
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2
Q

Helical viruses:

A

A few copies of a protein species bind to a helical ssRNA molecule, then more copies bind until the RNA is completely coated.

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3
Q

Icosahedral viruses:

A
  • Procapsid (prohead) — empty protein shell (with hole)
  • Filled with a copy of genome (through hole)
  • Modification to form mature capsid (close hole by the use of protein conformational change)
    - Needs chaperones from host cell
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4
Q

procapsid =

A

Empty shell w/ hole

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5
Q

capsid =

A

Filled shell w/ no hole

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6
Q

How does the virus tell which DNA or RNA to fill procapsid?

A
  • Signal sequences on genome is recognized by procapsid hole proteins
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7
Q 
(Genome Packaging)
How are virus genomes selected from all the cell and virus nucleic acids? (3)
- \_\_\_\_\_ \_\_\_\_ =
- The intermediate molecules...
- Some host nucleic acids are still...
A
  • Packaging signal = a specific sequence of viral genome recognized by virial proteins.
  • The intermediate molecules (template DNAs and RNAs) are not packed, the signals are masked by proteins.
  • Some host nucleic acids are still packed into virions, in terms of retreoviruses, some host tRNAs are important
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8
Q

Assembly mechanisms: (2)

A
  1. ) Simple viruses (ex: TMV) = can assemble by themselves in test tubes under the right condition (ex: pH, ions, etc.)
  2. ) Complex viruses (ex: herpes viruses and tailed phage) = need the environment of host cells — (directed assembly)
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9
Q

In vitro = outside of cells

In vivo = inside of cells

A

= outside of cells

= inside of cells

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10
Q

(Differences???)
Simple viruses:
Complex viruses:

A

can assemble spontaneously

needs host cells to assemble

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11
Q

Formation of virion membranes: (2)

A
  1. ) Budding through cell membranes

2. ) De novo synthesis of viral membranes

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12
Q

Host cells display…

- exit is…

A

…surface proteins

- …STILL part of assembly step

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13
Q

(De novo viral membrane synthesis)
Minority of viruses can…
- Some cases: the membrane forms…
- Other cases: the membrane forms…

A

…direct the synthesis of lipid membrane late in the replication cycle.

  • …virion envelope
  • …layer below the surface of the capsid
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14
Q

(Virion Exit from the infected cell)
Many viruses initiate:
- Many phages produce…
- Other phages synthesize…

A

cell burst (lysis)

  • …enzymes (lysins, such as lysozymes) that break bonds in the peptidoglycan of the host bacterial cell walls
  • …proteins that inhibit host enzymes with roles in cell wall synthesis (leads to weakening of the cell wall and ultimately to lysis)
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15
Q

Average yields of infectious virions per cell…

A

vary considerably

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16
Q

Many viruses do not…

A

lyse their host cells; instead, progeny virions are released from the cells over a period of time.

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17
Q

(+) ssRNA genome viruses has…

Retroviruses have…

A

…less steps

…more steps

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18
Q

Outcomes of infection for the host: (2)

A
  1. ) Productive
  2. ) Non productive
    - Become latent = virus genome stays with the cells perhaps for the lifetime, and even in the daughter cells.
    - Infection is abortive = neither productive or latent, due to virus genome mutations.
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19
Q

Productive infection =

A

= release of infective progeny virions from an infected cell.

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20
Q

Non productive infection can become

A

latent or abortive

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21
Q

latent (non productive) infection =

A

virus genome stays with the cells perhaps for the lifetime, and even in the daughter cells.

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22
Q

abortive (non productive) infection =

A

= neither productive or latent, due to virus genome mutations.

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23
Q

Factors affecting outcomes of infection: (4)

A
  1. ) Innate immunity in vertebrates
  2. ) Adaptive immunity in vertebrates
  3. ) RNA silencing
  4. ) Programmed cell death
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24
Q

Interferons =
& function =
& are part of…

A

= proteins synthesized and secreted by cells in response to virus infection.

= to protect adjacent cells from infection and to activate T cell-mediated immunity

…part of innate immunity

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25
Q

A potent trigger for interferon production is

A

dsRNA (produced by dsRNA viruses & ssRNA viruses as they replicate)

26
Q

After secretion, the interferon molecules…

A

…diffuse to nearby cells, where they can trigger various anti-viral activities by binding to interferon receptors.

27
Q
  • Interferons released from virus-infected cells bind to…

- If the cells become infected,

A
  • interferon receptors on other cells

- either block virus replication or kill the infected cells

28
Q

Anti-viral activities triggered by α- and β-interferons include: (3)

A
  1. ) Activation of genes that encode antiviral proteins
  2. ) Activation of NK cells (Innate/natural immunity)
  3. ) Induction of apoptosis
29
Q

Natural killer aka

A

“(NK) cells”

30
Q

NK cells are present where

A

throughout the body, but mainly in the blood.

31
Q

NK cells function (2)

A

They recognize changes in the surface molecules of virus-infected cells as a result of infection, then bind to them and kill them.
They also release γ-interferon, which activates macrophage

32
Q

Adaptive immunity (2)

A

antibodies

T cells

33
Q

Antibodies are

A

antigen-specific antibodies synthesized by plasma cells, which develop from a B cell after it has been stimulated by the antigen.

34
Q

B cell –> Plasma cell process requires

A

gene reorganization

35
Q 
(Consequences of antibody binding)
The antibody can coat...
- Allowing...
- Activate...
- Neutralize...
A

…can coat both virions and virus-infected cells, and this may lead to their destruction by a variety of mechanisms.

  • Allowing certain type of cells in immune system to attach to antibody-coated virions and cells to phagocytose them or kill them.
  • Activate complement proteins, inactivate viruses.
  • Neutralize virus infectivity.
36
Q

What are produced several days after antigenic stimulation?

A

effector T cells

37
Q

2 types of T cells & function:

A
  1. ) Helper T cells: trigger immune responses, e.g. trigger the production of B cells and cytotoxic T cells.
  2. ) Cytotoxic T cells: kill virus-infected cells.
38
Q

B cells –>

A

plasma cells –> antibodies

39
Q

T cells –> (2)

A

–> helper T cells –> T cells or B cells

or

–> cytotoxic T cells

40
Q

Plasma cells, helper T cells, and cytotoxic T cells can

A

remain in reserve

- next infection = quick immune response

41
Q

Some B cells and T cells can survive as

A

memory cells long after the first or subsequent encounters with the viruses.

42
Q

Memory cells =

A

returned to a resting state, (can be reactivated if they encounter the same antigen again)

43
Q
  • The outcome of infection of a vertebrate animal with a virus may depend on…
  • If immunological memory is present, then…
A
  • whether or not the host has immunological memory of the virus antigens.
  • signs and symptoms of disease are likely to be less severe, or totally absent.
44
Q

RISC function:

A

(part of RNA silencing)
cleaves target mRNA
- Completely stops RNA synthesis (self-defense mechanism)
- Our DNA is safe from this mechanism

45
Q

RISC only works if

A

VIRUS HAS dsRNA @ ANY POINT

46
Q

Once a lymphocyte has recognized a foreign antigen, it…

A

expands to eliminate the infection

47
Q

(Latent infections)

2 Occurrences:

A
  1. ) Virus DNA is integrated into a cell chromosome. After infection of the cell the virus genome is integrated into the genome of the host cell (ex: retroviruses)
  2. ) Virus DNA present as multiple copies of circular molecules.
48
Q

(Latent infections)

Temperate phage can be

A

both lytic and lysogenic (latent) infection

49
Q

Latent phage genome aka

A

“prophage”

50
Q

Latent phage genome (prophage) can be

A

either integrated into bacteria genome or non-integrated circular DNA

51
Q

Some virulent factors of bacteria are coded by

A

the temperate phage,

e.g. Shiga toxin

52
Q

(Latent infections)

When to enter productive stage? (4)

A
  1. ) A eukaryotic host cell moves into another phase of the cell cycle.
  2. ) The host cell is irradiated with ultra-violet light.
  3. ) A host organism becomes immunocompromised.
  4. ) The host cell becomes infected with a second virus that provides a function that the first virus lacks. satellite virus and helper virus, respectively.
53
Q

Satellite virus =

A

A defective virus that depends on a helper virus to provide one or more functions.

54
Q

Helper virus =

A

A virus that can provide function(s) missing from a defective virus, thereby enabling the satellite virus to complete its replication cycle.

55
Q

The satellite viruses are like

A

“parasites of the helper virus. “

56
Q

Co-infection with a satellite virus can

A

increase the severity of the infection than just a helper virus alone.

57
Q

Reasons for Abortive infections: (3)

A
  • concerning the cell,
  • the environmental conditions
  • and/or the virus.
58
Q

A virus may initiate…

…and…

A

productive infections in some cell types (permissive cells)…

…and abortive infections in other cell types (non-permissive cells)

59
Q

Productive infections =

& can cause…

A

Spread of infections within multicellular hosts

…& can cause disease

60
Q

Virus infections result in: (3)

A

No disease
Disease
Death

MIC 430 (22 decks)

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