adenovirus Flashcards
True or false: cells with only E1B will enter the cell cycle but they will end up dying
true
what do IVa2 and 52/55k do
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
is VARNA a coding sequence and what does it do
it is a non-coding sequence and it blocks the interferon pathway aka it blocks the immune response
True or false: E!A turns on expression of early promoters through 289R and 243R
true
true or false: E3 is not an immmune modulator
false: he is an immune modulator
what does 33k and 100k do
they are chaperones/scaffolds for capsid assembly
what do 11.6k and orf 3/4 do?
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
why did richard roberts and philip sharp win the noble prize
they won it in 1993 for their discoveries of split genes
true or false: the viral genome of adenoviruses has cellular histones
true but it also has viral proteins on their genomes
why does a virus want oncogenes
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
Top which family p300 and CBP are in
HATS
what is the main role of the RB family
it is a tumor suppressor, if mutated=cancer
what happens if there are mutations in CR1 and 2
the proteins made won’t bind to RB and then E1A can’t keep the S phase
why is the N terminus important in adenoviruses
if it gets peeled off E1A is less effective= the TFs produced have more difficulty activating viral genes and the S phase
Why is RB blocks at the G1?
-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
What happens if E2F is turned on?
things that are regulated by it will also be turned on like DNA pol and genes for nucleotide synthesis
How does E1A inhibits cell differenciation?
-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
what are the most important proteins for replication in adenovirus
-viral dna pol
-terminal protein
-dna binding protein
explain how adenovirus replicates
adeno virus ppt page 25
what are the roles of the terminal repeats in adeno virus
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
true or false: there is always the tripartite leader in the mrna of adenovirus
true
how is the adenovirus able to take one long strand of DNA and then make a lot of proteins
alternative splicingggg
what is the role of the p14 arf gene
-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
how does E1A induce apoptosis
it binds to MDM and then p53 is stable= apoptosisss
what is the role of E1B-55k gene
-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
true or false: there are clinical trials for making adenoviruses into oncolytic virus
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
which gene in adenoviruses has homology with cellular bcl2
-E1B-19k so it inhibits cellular apoptosis
it kinda shifts the cellular balance so that bax and p53 are less powerful
hat is the role of VA RNA
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
t is the role of E3 in adenoviruses
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
