Lecture 11 Flashcards
What are adenoviruses responsible for?
respiratory infections like the cold
when were adenoviruses discovered
in the 50’s
What happenend when adenoviruses were introduced into rodents
they developed cancers
true or false: adenoviruses cause cancer in humans
false they don’t
-in rodents their genes are oncogenic because they promote growth
-in humans when the virus replicates, it kills the cell
who are more susceptible to adenoviruses
people living in close quarters like kids in boarding schools and military
stats about adenoviruses
*Non-enveloped
*Icosahedral
*90 nm in diameter
*Genome: dsDNA
35-45 kb
linear
which covid vaccine was due to an adenovirus?
astrazenequa
True or false: adenoviridae co-evolved with vertebrates not too long ago
falseeee
adenoviridae co-evolved with vertebrates for eons
qhich genus of adeoviridae are responsible for human infections?
mastadenovirus
Which of these are not caused by adenovirus:
Acute Respiratory Illness
Pharyngitis
Gastroenteritis
Conjunctivitis
Pneumonia
Influenza
Keratoconjunctivitis
Acute Haemorrhagic Cystitis
Hepatitis
influenza
which adenovirus serotypes are responsible for the common cold?
2 and 5
Where do adenoviruses replicate?
in the nucleus
it also replicates quickly
Where does adenoviruses replicate best?
in epithelial cells
how do we purify adenovirus
using a CsCl gradient and we spinnnn it
True or false: adenovirus has to bring lots fo proteins in order to replicate
false: it only brings with it the structural components and the genome
True or false: adenovirus is tightly packed and it is thanks to protein VII
true
it is like an histone like protein that condense the genome
what is the role of protein VIII in adeno viruses
cements the capsid together from the inside
hat is the role of protein VI
it links the core to the capsid
True or false: the genome of adenoviruses is temporaly regulated
true
what does E1A do?
It is a potent TF, it activated E1B, E3, E2Aand B
how did we discover splicing?
with the usage of adenoviruses
-They basically looked at the EM of mRNA and saw it looping out
Do adenoviruses have inverted terminal repeats
yes
Why does a virus want oncogenes? more specifically adenoviruses
because iy this case epithelial cells don’t really replicate, they already are differentiated aka they don’t really divide
-viruses develop proteins that regulate replication and that will push these cells to the S phase even though they don’t have active DNA replication
Why do adenoviruses produce an excess quantity of fibers?
because thet use them to bind to the CAR receptors so that they don;’t bond to themselves and block entry for the virus
how does adenoviruses enter the cell
through 2 interactiosn:
-first with the car receptors
-on the penton there is this RGD loop(amino acid sequence) and this will bind to the integrins present on the cell surface
=multiple interactions
how does adenoviruses enter the cell
through 2 interactiosn:
-first with the car receptors
-on the penton there is this RGD loop(amino acid sequence) and this will bind to the integrins present on the cell surface
=multiple interaction
what causes the disassembly of the capsid
-acidification in the endosome activates a protease which digests protein VI=disassembly of the outer capsid
how does adenovirus leaves the endosomelea
it leaves through phospholipase activity into the cytoplasm->nucleus
what are the 2 main product of E1A
289R and 243R
what is present on 289R but not 243R and what does it do
CR3:
-it is important for turning on the other TFs
-it binds TBP (tata box binding protein) and ATF (which binds in a sequence specific way to different promoters
when these 2 are bound, it hyperactivats the transcription of the DNA
true or false: E1B/E3/E4 all have ATF binding sites
true
E1A binds to… and … whic…
E1A binds tyo TBP and ATF forms like this bridge and hyperactivates the other TFS
what do pRB,p107 and p130mbind to
CR1 and Cr2
E2 is responsible for binding to them
important for driving the cells to the S phase
True or false: E1A proteins activate E2F transcription
and explain how it works
true
usually Rb is always bound to E2F= represses S phase genes but E1A will bind to RB and then E2F can be free to activate S phase
