Greber Flashcards
What are the three hallmarks of persistant infections?
- the primary infection is not cleared by the immune system
- infectious particles continue to be produced.
- Viral genome is still detected, even tho viral proteins aren’t.
What strategies are very efficient to get high levels of persistance ?
Infecting certain cell types, e.g. immune cells.
Antigenic escape.
IFN antagonism.
Is the oncogenic potential of HPVs equal ?
No, type specific: some are high risk (16) and others low (6) or medium
HPV 16: what kind of genome ?
Circular DNA.
How is HPV16 causing sometimes cancer ?
It’s an episome that can integrate, and sometime does it in the E2 region - this protein is supposed to repress the transforming proteins E6 and E7. They’re then overproduced and case cancer formation.
What's: E1 ? E2 ? E6 ? E7 ?
E1: helicase.
E2: protein regulator affecting E1, but E6 and E7.
E6: p53 blocker, activates telomerases.
E7: Forces S phase.
Primary hosts of HPVs ?
Mammals and birds. Very common.
What are the diseases caused by AdV ?
Respiratory Conjunctivitis Intestinal tract Kidney and Urinary tract Obesity
site of replication of AdV?
Nucleus duuuhhh
What does a helper virus do ?
Provides proteins etc to help replication but isn’t packaged into the virion - its genome however has the packaging sequence.
What are the three types of cell surface binding factors ?
Primary receptor: that’s the thing binding to the virus and allowing his entry.
Attachment factor: enhances the access to the receptor.
Facilitator: surface factor that doesn’t bind the virus BUT enhances infection indirectly.
During endocytosis, AdV fibers dissociate. How and what does it do?
Interaction with the receptor (CAR and integrin) causes mechanical forces to pluck the fibers out of the particles, realeasing some protein VI.
VI makes small pores, inducing a Ca current and recruiting enzymes that convert stuff into ceramide, the facilitator, that enables endocytosis and escape from endosome.
What happens after exit from the endosome for AdV?
AdV uses microtubules to travel to the nuclear envelope. In this process, follows a progressive decapsidation in a strict order, finalised only AFTER docking to the nuclear pores. Failing to do so will just release dsDNA in the cytoplasm and get cGASsed.
5 steps of AdV replication.
- Entry, uncoating, nuclear import
- Immediate gene expression
- Early gene expression and replication
- Late gene expression
Assembly - Release
What favors AdV persistence in human?
Absence of lysis.
What is the major AdV viral transactivator and what does it do ?
It’s E1A, it controlls all the AdV promoters, promotes division in quiescent cells AND suppresses the immune response.
What particular interaction of E1A allows persistance?
As E1A is being made, it can activate an E3 promoter that causes the splicer XBP1s protein that keeps persitant levels of E1A in the cell in the presence of IFN.
Picornas: structure?
Naked icosahedral capsid.
Picornas are still sensitive to some stuf: what?
Temperature, javel, and other strong acidic chemicals.
From subunits to capsid: how does it go?
VP0, 1 and 3 assembles as protomers.
5 protomers -> pentamers
12 pentamers -> Provirion
Picorna genome?
Positive sense RNA virus of about 7kb with a single ORF
What’s the transmission mode of these picorna ?
Fecal Oral transmission or Aerosol.
What’s the physiopathology of picornas ?
If they cross into the blood circulation from intestinal OR airway infections, they can cause skin issues or CNS infections (meningitis and encephalitis). And paralysis etc (polyo)
Polioviruses have two vaccines: which ones and diff?
Salk vaccine, inactivated vaccine.
Sabin: attenuated vaccine.
