Lec 5 - Exocytosis and genome recognition Flashcards
what phase in one step growth curve does exocytosis happen
rise period
each virus has avg burst size
how to naked viruses leave cell
once cpasid is made = cell lysis
how do memb bound viruses leave the cell
need to acquire memb
then leave via budding (maybe secondary cell lysis will occur)
what do bacteriophage release to get out of cell
cytolytic molecules
remember - peptidoglycan cell wall more robust than eukaryotic, so cell lysis needs to happen for it to leave
name the primer on poilio that allows RNA replication
VPG
what does polio P1 encode for
capsid subunits
V1 V2 etc
what does polio P2 encode for
protease 2A and toxin 2A
what does polio P3 encode for
replicase
VPG
protease
what does 5’ end of mRNA in cell have that allows ribosomes to recognise
eIF4F complex
how does polio stop the cells protein synthesis
cleaves eIF4F complex with its 2A protease
means cellular RNA cant bind ribosomes
how does polio ensure that the cellular ribosomes can recognise its RNA
has IRES sequence in its genome
which polio protein alter membrane permeability of host
2B toxin
how does influenza virus acquire its membrane
cell’s plasma memb
how does herpes virus acquire its membrane
internal membranes of secretory pathway
what protein does coronavirus use to acquire its secretory membranes
E1
lots deposited in ER
herpes virus: protein used to get nucleocapsid out of nucleus
UL34
UL31
these 2 catalyse budding
and tegument proteins
herpes virus: which proteins allow uptake of NC into golgi
gE gI and gM
tegument proteins will bind to these and its taken into golgi
what needs to be cleaved in HIV to make it infectious
Gag polyprotein
(cleaved by HIV protease - used as drug target)
what do viruses have that allows it to distinguish viral genomes from cellular gneomes
packaging signals
packaging signal in SV40
sp1
packaging signal in herpes virus
pac1 and pac2
what is a concatemer
long strand of DNA, lots of copies of the viral genome
influenza has a segmented genome (8 segments) - how does it ensure capsid interacts with correct genomes
each segment has unique packaging signal
so its not random (which what was originally thought)
