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MICRO > banfield lectures 8/9 > Flashcards

banfield lectures 8/9 Flashcards

1
Q

t or f, growth of a virus in a cell depends on if the virus is cytolytic of non-cytolytic

A

true. cytolytic viruses grow quickly and cause cell lysis quickly

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2
Q

what are common cytopathic effects of viruses (5)

A
  1. inhibit protein synthesis
  2. damage cell lysosomes (release digestive enzymes)
  3. alter PM
  4. viral inclusions
  5. transfer host into malignant cell
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3
Q

explain the general idea behind immune cells kiling infected cells

A
  1. viral envelope proteins are expressed onto the infected cel surface
  2. antibodies recognize these and bind them which flag other cells to come.
  3. the antibodies also fix complement (series of proteins that can make the cell lyse
  4. the attracted cells such as NK cells can come and kill the infected cell too.
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4
Q

t or f, NK cells are adaptive immune cells

A

FALSE, they are innate cells that recognize a wide range of foreign material within the body

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5
Q

t or f, necrosis is highly regulated and apoptosis is passive

A

false,
apoptosis is a highly regulated process.
necrosis is passive

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6
Q

what is necrosis

what causes it, what is the result

A

cell death that results from external factors such as physical damage due to pH change, temp change, chemical trauma, etc.
The end result of necrosis is loss of membrane integrity and cell death (cytoplasm spills out)

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7
Q

the cytoplasmic leakage due to necrosis is good and bad, why?

A

the leaked content is a seen as danger signal by the immune system. As a result a robust inflammatory response occurs and initiation of an adaptive immune response begins. (good)

Bad –> the response is immunopatholigic meaning the immune response leads to symptoms. additionally inflammation of the brain is dangerous.

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8
Q

what is apoptosis?

A

programmed cell death. This is accomplished by a cascade of biochemical actions that cause cell fragmentation. phagocytes engulf these fragments.

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9
Q

t or f, the cell membrane remains intact during apoptosis

A

true, unlike necrosis

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10
Q

t or f, apoptosis results in a pro-inflammatory response

A

false! again unlike necrosis (recall inflammation is a result of leaked cytoplasm. This leakage is not apparent in apoptosis)

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11
Q

t or f, apoptosis is a natural process

A

true, it occurs when a cell is misbehaving. Therefore in cells that have viruses in them, apoptosis can occur

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12
Q

when macrophages and phagocytes engulf infected cell fragments via apoptosis, this action aids in the adaptive response initiation… why?

A

the engulfment of the fragments also engulfs the foreign bodies on the cell surface and the antigens which indicate the virus .

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13
Q

some viruses have developed ways to circumvent apoptosis, others have found ways to induce it. Why?

A

some viruses have made sure it does not happen so that the virus can proliferate in the cell. other viruses induce it by means to spread itself. (important: the timing is crucial, if the virus replication is not complete the apoptosis will be beneficial to the host rather than the virus

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14
Q

explain interplay between virus disease and host defence (balance)

A

viruses need a proper balance between the severity of the disease they produce and the ability for the host to clear the virus. If they are too severe = no more hosts = virus dies.
if host response is too good = virus dies.

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15
Q

the main differences between innate and adaptive responses?

A

innate –> occurs in minutes to hours. non- specific response. it restricts viral amplification

adaptive –> days to weeks to develop. critical for clearing the infection. Pathogen specific.

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16
Q

t or f, the adaptive response can also occur within minutes of infection

A

true, if the virus has infected you already, the adaptive response is primed and ready to go. (how vaccines work)

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17
Q

what is the hierarchy of immunity

A
  1. intrinsic
  2. innate
  3. adaptive
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18
Q

what are the intrinsic antiviral cell mechanisms

A

these are defined as pre- existing defences in the body (not induced). this is not the same as the skin/external mucus. this is the first line of cellular defence

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19
Q

intrinsic defence: autophagy

A

this is when the cell is lacking AA’s. the cell eats one of its mitochondria to acquire AA’s for protein synthesis.

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20
Q

intrinsic defence: xenophagy

A

this is when the cell eats foreign substances to acquire needed AA’s

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21
Q

intrinsic defence: Host restriction factors

A

these are retrovirus specific factors (recall retroviruses are + RNA strand viruses that replicate through a DNA intermediate!!) these host restriction factors inhibit the DNA intermediate formation

22
Q

intrinsic defence: epigenetic transcriptional silencing

A

histone modifications silence viral genomes. (e.g. histones bind herpes virus DNA and cause it to condense a lot preventing transcription )

23
Q

true or false, apoptosis is an intrinsic response

A

true (its already happening naturally before infection)

24
Q

what are the 4 main components of the innate response?

A
  • cytokines
  • NK cells
  • complement
  • sentinel cells (i.e. macrophages)
25
Q

what are cytokines

A

soluble proteins secreted by immune cells which have many affects (cell communication, initiation of adaptive response, etc. )

26
Q

what are the 4 classes of cytokines?

A
  1. pro-inflammatory: promote leukocyte activation
  2. anti-inflammatory: return cells to basal state
  3. chemokines: attractant molecule that recruits immune cells.
  4. interferons :
27
Q

what is NF-Kappa B?

A

a very important transcription factor that leads to cytokine production.

28
Q

what is interferon

A

a cytokine released by infected cells which acts on other cells to help them prep for a potential viral infection (anti-viral state)

29
Q

what two transcription factors are responsible for IFN

A

IRF3 and IRF7
(interferon regulatory factor)
note: these molecules are turned on in cells with the virus so that IFN can be produced. this is different then genes that IFN stimulates in neighbouring cells.

30
Q

t or f, IFN is an anti-viral molecule

A

false, it is just a signalling molecule

31
Q

when interferon binds a cell, there is potential for an increase in expression in 300 genes.. t or f

A

true, typically 50-100 of them are expressed upon binding

32
Q

what are ISG’s

A

interferon stimulated genes. These are responsible for turning on the anti-viral state.

33
Q

interlude: the expression of IFN in infected cells (IFR3/7) and the expression of genes in neighbouring cells (ISG’s) due to IFN are different. don’t mix these up

A

:) fuck u

34
Q

what are PAMPS (what are some examples too)

A

PAMPS are pathogen associated molecular patterns. PAMPS incluce LPS, dsDNA, ssRNA, lack of methylation

35
Q

t or f, PAMPS are specific to viruses

A

false, many things have characteristic PAMPs

36
Q

why are dsDNA and ssDNA considered PAMPS?

A

location: ssRNA does not belong in an endosome and dsDNA does not belong as a free floating molecule.

37
Q

where are PAMP receptors located?

A
  • cell surface
  • endosome lumen
  • in cytoplasm
38
Q

What are the two PAMP receptors?

A
  1. toll-like receptors

2. cytoplasmic RNA helicases

39
Q

Where are toll-like PAMP receptors found?

A
  1. they are expressed predominantly in antigen-presenting cells such as dendritic cells and macrophages. .
  2. these cells are typically in the PM or endosomal lumen
40
Q

Where are the cytoplasmic RNA helicases found? what are they called?

A

there are two Cytoplasmic RNA helicases
1. RIG-I
2. mda5
They are widely expressed in tissues and activate upon dsRNA binding

41
Q

t or f, a 5’ phosphate group with no cap indicates a molecule is foreign

A

true

42
Q

what does RIG-I detect?

A

detects dsRNA, ssRNA with 5’ phosphate

43
Q

what does mda5 detect?

A

only dsRNA

44
Q

What is the JAK/STAT pathway?

A

this is the pathway taken when IFN (and other cytokines) binds the outside of the cell.

45
Q

what are STAT proteins? how many exist?

A

these are cytoplasmic transcriptional factors that are activated upon IFN binding. There is 7. In their activation they dimerize into homo and heteromers making many combinations possible.

46
Q

Explain the JAK / STAT pathway until STAT binding (4) (including stat binding)

A
  1. IFN binds a transmembrane receptor with two components and two JAK proteins on the intracellular side
  2. upon binding, the receptor components come together which brings the JAKS together.
  3. The JAKS are kinase molecules which phosphorylate the end of the receptor
  4. this acts as a docking site for STATS proteins to bind the end where the phosphorylation has occured.
47
Q

Explain the JAK / STAT pathway after STAT binding (3)

A
  1. now the STAT TF’s have been recruited to the phosphorylated receptor, the JAKS phosphorylate the recruited STATS.
  2. once phosphorylated, the STATS dimerize (bind each other) giving rise to many STAT dimer possibilities
  3. this dimer gets translocated to the nucleus where the TF turns on ISG’s
48
Q

explain briefly the IFN specific JAK / STAT pathway.

A
  1. IFN 1 binds the receptor
  2. JAK1 and TYK2 (JAK kinases) phosphorylate the receptor tail which leads to STAT phosphorylation
  3. STAT 1 and STAT2 heterodimerize
  4. IRF9 binds the dimer and aids it into the nucleus
  5. this complex sits on DNA at ISG’s causes transcription.
49
Q

what are the results of IFN receptor stimulation and ISG activation?

A 
the IRF9 (STAT1/2) complex (collectively called ISGF3) activates ISG's which cause the production of many proteins (many unknown functionality). 
The net response is the cell going into an "anti-viral" state. In this state, if the cell gets infected at all by the virus it will immediately begin apoptosis and die.
50
Q

what is PKR?

A

one of the proteins translated for the antiviral state. (probs don’t need to know)

MICRO (28 decks)

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