MIC 430 > Lec 7: Assembly & Exit > Flashcards

Lec 7: Assembly & Exit Flashcards

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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
A potent trigger for interferon production is
dsRNA (produced by dsRNA viruses & ssRNA viruses as they replicate)
26
After secretion, the interferon molecules...
...diffuse to nearby cells, where they can trigger various anti-viral activities by binding to interferon receptors.
27
- Interferons released from virus-infected cells bind to... | - If the cells become infected,
- interferon receptors on other cells | - either block virus replication or kill the infected cells
28
Anti-viral activities triggered by α- and β-interferons include: (3)
1. ) Activation of genes that encode antiviral proteins 2. ) Activation of NK cells (Innate/natural immunity) 3. ) Induction of apoptosis
29
Natural killer aka
"(NK) cells"
30
NK cells are present where
throughout the body, but mainly in the blood.
31
NK cells function (2)
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
Adaptive immunity (2)
antibodies | T cells
33
Antibodies are
antigen-specific antibodies synthesized by plasma cells, which develop from a B cell after it has been stimulated by the antigen.
34
B cell --> Plasma cell process requires
gene reorganization
35
``` (Consequences of antibody binding) The antibody can coat... - Allowing... - Activate... - Neutralize... ```
...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
What are produced several days after antigenic stimulation?
effector T cells
37
2 types of T cells & function:
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
B cells -->
plasma cells --> antibodies
39
T cells --> (2)
--> helper T cells --> T cells or B cells or --> cytotoxic T cells
40
Plasma cells, helper T cells, and cytotoxic T cells can
remain in reserve | - next infection = quick immune response
41
Some B cells and T cells can survive as
memory cells long after the first or subsequent encounters with the viruses.
42
Memory cells =
returned to a resting state, (can be reactivated if they encounter the same antigen again)
43
- The outcome of infection of a vertebrate animal with a virus may depend on... - If immunological memory is present, then...
- 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
RISC function:
(part of RNA silencing) cleaves target mRNA - Completely stops RNA synthesis (self-defense mechanism) - Our DNA is safe from this mechanism
45
RISC only works if
VIRUS HAS dsRNA @ ANY POINT
46
Once a lymphocyte has recognized a foreign antigen, it...
expands to eliminate the infection
47
(Latent infections) | 2 Occurrences:
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
(Latent infections) | Temperate phage can be
both lytic and lysogenic (latent) infection
49
Latent phage genome aka
"prophage"
50
Latent phage genome (prophage) can be
either integrated into bacteria genome or non-integrated circular DNA
51
Some virulent factors of bacteria are coded by
the temperate phage, | e.g. Shiga toxin
52
(Latent infections) | When to enter productive stage? (4)
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
Satellite virus =
A defective virus that depends on a helper virus to provide one or more functions.
54
Helper virus =
A virus that can provide function(s) missing from a defective virus, thereby enabling the satellite virus to complete its replication cycle.
55
The satellite viruses are like
"parasites of the helper virus. "
56
Co-infection with a satellite virus can
increase the severity of the infection than just a helper virus alone.
57
Reasons for Abortive infections: (3)
- concerning the cell, - the environmental conditions - and/or the virus.
58
A virus may initiate... | ...and...
productive infections in some cell types (permissive cells)… | ...and abortive infections in other cell types (non-permissive cells)
59
Productive infections = | & can cause...
Spread of infections within multicellular hosts | ...& can cause disease
60
Virus infections result in: (3)
No disease Disease Death
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