adenovirus Flashcards

1
Q

True or false: cells with only E1B will enter the cell cycle but they will end up dying

A

true

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2
Q

what do IVa2 and 52/55k do

A

IVa2 is an intermediate gene and 52/55k is a late gene
basically what they do is they are atpases motors that will help put the viral genome into the capsid

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3
Q

is VARNA a coding sequence and what does it do

A

it is a non-coding sequence and it blocks the interferon pathway aka it blocks the immune response

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4
Q

True or false: E!A turns on expression of early promoters through 289R and 243R

A

true

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5
Q

true or false: E3 is not an immmune modulator

A

false: he is an immune modulator

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6
Q

what does 33k and 100k do

A

they are chaperones/scaffolds for capsid assembly

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7
Q

what do 11.6k and orf 3/4 do?

A

INDUCE APOPTOSIS AT THE completion of the viral life cycle
-lysys=helps the cell go out
if no 11.6k= cells are full of virus but it can’t get out

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8
Q

why did richard roberts and philip sharp win the noble prize

A

they won it in 1993 for their discoveries of split genes

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9
Q

true or false: the viral genome of adenoviruses has cellular histones

A

true but it also has viral proteins on their genomes

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10
Q

why does a virus want oncogenes

A

because depending on where the virus infect the cells ex: epithelial cells
they don’t replicate, they don’t divide because they are already differentiated
viruses develop proteins that regulate replication and push the cells into S phase

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11
Q

Top which family p300 and CBP are in

A

HATS

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12
Q

what is the main role of the RB family

A

it is a tumor suppressor, if mutated=cancer

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13
Q

what happens if there are mutations in CR1 and 2

A

the proteins made won’t bind to RB and then E1A can’t keep the S phase

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14
Q

why is the N terminus important in adenoviruses

A

if it gets peeled off E1A is less effective= the TFs produced have more difficulty activating viral genes and the S phase

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15
Q

Why is RB blocks at the G1?

A

-it is between the “real” start point aka go or no go decision
-RB is the real gatekeeper of the cell cycle progression
boundary between G1 and S phase
-sensitive to growth factors

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16
Q

What happens if E2F is turned on?

A

things that are regulated by it will also be turned on like DNA pol and genes for nucleotide synthesis

17
Q

How does E1A inhibits cell differenciation?

A

-through binding of p300 and CBP
-p300 and CBP (cAMP binding proteins) are related cellular proteins which have histone-acetyltransferase (HAT) activity
-Acetylation of histones induces chromatin modification resulting in increased gene expression due to relaxing of histone/DNA complex formation
- Acetylation of histones results in the expression of genes involved in various cellular functions including cell differentiation.
-Differentiation mediates cell cycle arrest

18
Q

what are the most important proteins for replication in adenovirus

A

-viral dna pol
-terminal protein
-dna binding protein

19
Q

explain how adenovirus replicates

A

adeno virus ppt page 25

20
Q

what are the roles of the terminal repeats in adeno virus

A

it is so that the og strand that is left alone can bp with itself to make some type of loop then the DNA pol can synthesize a new strand

21
Q

true or false: there is always the tripartite leader in the mrna of adenovirus

A

true

22
Q

how is the adenovirus able to take one long strand of DNA and then make a lot of proteins

A

alternative splicingggg

23
Q

what is the role of the p14 arf gene

A

-tumor suppresor
-when E2F is upregulated it’ll recognize that it is def sus
-p14 arf will then bind to MDM (which is usually bound to P53 aka best tumor suppressor and MDM destabilize the p53
-when 53 is off from MDM it is more stable and will induce apoptosissss
-if there is like UV or weird chemicals then it’ll also stabilize p53

24
Q

how does E1A induce apoptosis

A

it binds to MDM and then p53 is stable= apoptosisss

25
Q

what is the role of E1B-55k gene

A

-it inhibits p53 through complex formation
-it binds to p53 and then there is cell survival in presence of E1A
-because when you wanna infect a cell you need E1A for 0starting S phase and then you can inhibit p53

26
Q

true or false: there are clinical trials for making adenoviruses into oncolytic virus

A

yes
you modify the viorus so that there is no E1B 55k so it can’t mess with p53=only replicates in cancer cells where p53 is mutated
-it’ll then replicate and then will lyse the cells

27
Q

which gene in adenoviruses has homology with cellular bcl2

A

-E1B-19k so it inhibits cellular apoptosis
it kinda shifts the cellular balance so that bax and p53 are less powerful

28
Q

hat is the role of VA RNA

A

it binds to PKR which is important for viral sensing, if it sense drrna it’ll phosphorylate then phosphorylate elF2a which’ll shut down the translation
-by binding tightly to PKR it inhibits it
-it also binds to dicer which is important for making micrornas and exportin-s so it blocks the nuclear export of pre-mirna
-dicer inhibits viral replication of adenovirus
-pkr also binds to dicer so no mirna is made

29
Q

t is the role of E3 in adenoviruses

A

the E3 region is in charge of downregulation the immune response
-it downregulates the TNF receptor and TRAIL which are involved with T cell killing virus infected cells
-GP19k also internalizes the MHC which is usually used by infected cells to show off peptides to say that they are infected